Kidney Damage Holistic Treatment

Kidney Function Restoration Program

You'll Learn: This Delicious Super Food Straight From Your Fridge is Loaded With Special Compounds that reverse free radical kidney cell damage. This food (freely available from a grocery store near you) has tremendous antioxidant activity. Antioxidants soak up and destroy free radicals. Free radicals are what cause much of the damage in inflammatory, degenerative and kidney diseases. The Popular Test Used By Korean Doctors which is barely used in America to check for potent kidney destroying toxins. Ridding your kidneys of these toxins is very easy but you first have to discover if you have them. The Essential Fatty Acid has shown in hundreds of people through multiple studies to put out inflammation and correct heart complications seen in kidney disease. This Miracle Nutrient Featured in the prestigious medical Journals of Nephron, Clinical and Experimental Nephrology, Renal Physiology and other double blind studies to produce significant results in reversing kidney problems, lowering blood pressure and study participants reported a boost in energy and focus. This Naturally Occurring Amino Acid Discovered by Russian scientists in the 1920s and published in over 100 studies worldwide has shown to slow down and possible stop kidney disease, improve your red blood cells (which are malfunctioning in renal disease), and increase mood and decrease fatigue. The National kidney Disease Foundation recommends suffers of renal disease get tested and supplement their diet with this nutrient. But very few medical professionals are actually doing this. The Delicious Tropical Fruit that is cultivated in the Caribbean, South America, Asia, Australia and parts of Africa that is toxic and poisonous to an injured kidney. If you have any decrease in kidney function you must stay far away from this fruit that is abundant in the spring and summer seasons. Read more here...

Kidney Function Restoration Program Overview


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Assessment of Kidney Function in the Elderly

Kidney function commonly declines with age, although not universally (6-9). Approximately one-third of elderly adults do not exhibit an age-related decline in kidney function (6). This has led to the suggestion that a decline in GFR is not a normal accompaniment of aging, but rather due at least in part to concomitant hypertension, cardiovascular disease, and diabetes mellitus. By the age of 80 years, mean GFR, depending on how it is measured or estimated, is approximately 50-80 mL min, compared to 120 mL min or greater in subjects in their 20s-40s. The prevalence of CKD in 65-74 year olds and individuals 75 years and greater is increasingly steadily, and there are more patients 70 years or older starting dialysis each year than any other age group (10). Despite this reduced level of GFR with advanced age, serum creatinine levels tend to remain relatively unchanged or increase only modestly over time in the absence of other conditions, a reflection of the reduced muscle mass that...

Rationale For Insulinlike Growth Factor I Igfi In Acute Renal Failure

Over- and underexpression of IGF-I, this is the first growth factor that has been used in clinical trials for kidney disease. Listed above are a variety of studies of the effects of IGF-I in humans. This peptide has now been examined in several published studies of both acute and chronic renal failure. Additional studies are currently in progress. In the area of acute renal failure there are now two reported trials of IGF-I. In the initial study IGF-I or placebo was administered to patients undergoing surgery involving the suprarenal aorta or the renal arteries. This group was selected as it best simulated the work that had been reported in animal trials of ischemic acute renal injury. Fifty-four patients were randomized in a double-blind, placebo-controlled trial of IGF-I to prevent the acute decline in renal function frequently associated with this type of surgery. The primary end-point in this study was the incidence of renal dysfunction, defined as a reduction of the glomerular...

Nutrition In Acute Renal Failure

Nutritional goals in patients with acute renal failure (ARF). The goals of nutritional intervention in ARF differ from those in patients with chronic renal failure (CRF) One should not provide a minimal intake of nutrients (to minimize uremic toxicity or to retard progression of renal failure, as recommended for CRF) but rather an optimal amount of nutrients should be provided for correction and prevention of nutrient deficiencies and for stimulation of immunocompetence and wound healing in the mostly hypercata-bolic patients with ARF 1 .

Rationale For Organized Approach To Acute Renal Failure

PRESENTING FEATURES OF ACUTE RENAL FAILURE Rationale for an organized approach to acute renal failure (ARF). An organized approach to the patient with ARF is necessary, as this disorder is common and is caused by several insults that operate via numerous mechanisms. Successful amelioration of the renal failure state depends on early identification and treatment of the cause of the disorder 1-7 . If not diagnosed and treated and reversed quickly, it can lead to substantial morbidity and mortality. Presenting features of acute renal failure (ARF). ARF usually comes to clinical attention by the finding of either elevated (or rising) blood urea nitrogen (BUN) or serum creatinine concentration. Less commonly, decreased urine output ( less than 20 mL per hour) heralds the presence of ARF. It is important to acknowledge, however, that at least half of all cases of ARF are nonoliguric 2-6 . Thus, healthy urine output does not ensure normal renal function. Rarely, ARF comes to the attention of...

Acute Glomerulonephritis

DIAGNOSIS OF A POSSIBLE ACUTE GLOMERULAR PROCESS AS THE CAUSE OF ACUTE RENAL FAILURE Sudden onset of edema, dyspnea Systemic disorder (eg, lupus erythematosus, Wegener's granulomatosis, Goodpasture's syndrome) No evidence of other causes of renal failure Diagnosis of a possible acute glomerular process as the cause of acute renal failure (ARF). Acute glomerulonephritis is a relatively rare cause of ARF in adults. In the pediatric age group, acute glomerulonephri-tis and a disorder of small renal arteries (hemolytic-uremic syndrome) are relatively common causes. This figure depicts the historical, examination, and laboratory findings that collectively may support a diagnosis of acute glomerulonephritis as the cause of ARF 16, 17 .

Acute renal failure related to pregnancy

133 Renal failure 301 septic abortion and massive haemorrhage (traditionally caused by placental abruption, although any cause of hypovolaemia may be followed by renal failure). Other important causes include pyelonephritis, drug reactions (especially non-steroid anti-inflammatory drugs NSAIDs ), acute fatty liver and incompatible blood transfusion. In most cases, ARF is caused by acute tubular necrosis, although cortical necrosis has been seen after abruption and pre-eclampsia. Problems are those of ARF generally, especially related to fluid balance and the apparently increased susceptibility of pregnant women to developing pulmonary oedema.

Diagnosis Of Possible Acute Interstitial Nephritis As The Cause Of Acute Renal Failure

Of renal failure (see Fig. 12-16) Diagnosis of possible acute interstitial nephritis as the cause of acute renal failure (ARF). This figure outlines the historical, physical examination and other investigative methods that can lead to identification of acute interstitial nephritis as the cause of ARF 18 .

First Step In Evaluation Of Acute Renal Failure

Disorders that suggest or predispose to renal failure hypertension, diabetes mellitus, human immunodeficiency virus, vascular disease, abnormal urinalyses, family history of renal disease, medication use, toxin or environmental exposure, infection, heart failure, vasculitis, cancer Disorders that suggest or predispose to volume depletion vomiting, diarrhea, pancreatitis, gastrointestinal bleeding, burns, heat stroke, fever, uncontrolled diabetes mellitus, diuretic use, orthostatic hypotension, nothing-by-mouth status, nasogastric suctioning Disorders that suggest or predispose to obstruction stream abnormalities, nocturia, anti-cholingeric medications, stones, urinary tract infections, bladder or prostate disease, intra-abnominal malignancy, suprapubic or flank pain, anuria, fluctuating urine volumes Symptoms of renal failure anorexia, vomiting, reversed sleep pattern, puritus First step in evaluation of acute renal failure. SECOND STEP IN EVALUATION Second step in evaluation of acute...

Biocompatible Membranes In Intermittent Hemodialysis Ihd And Acute Renal Failure Arf Effect On Outcomes

Biocompatible membranes in intermittent hemodialysis (IHD) and acute renal failure (ARF) effect on outcomes. The choice of dialysis membrane and its influence on survival from ARF has been of major interest to investigators over the last few years. While the evidence tends to support a survival advantage for biocompatible membranes, most of the studies were not well controlled. The most recent multicenter study showed an improvement in mortality and recovery of renal function with biocompatible membranes however, this effect was not significant in oliguric patients. Further investigations are required in this area. NS not significant.

Determinant Mechanisms For Outcomes Of Acute Renal Failure

Mechanisms by which growth factors may possibly alter outcomes of acute renal failure (ARF). Epidermal growth factor, insulin-like growth factor, and hepatocyte growth factor (HGF) have all been demonstrated to improve outcomes when administered in the setting of experimental ARF. While the results are the same, the respective mechanisms of actions of each of these growth factors are probably quite different. Many investigators have examined individual growth factors for a variety of properties that may be beneficial in the setting of ARF. This table lists several of the properties examined to date. Suffice it to say that the mechanisms by which the individual growth factors alter the course of experimental ARF is still unknown.

Clinical Use of Growth Factors in Acute Renal Failure

Body weights of rats with ischemic acute renal failure (ARF) treated with insulin-like growth factor (IGF-I) or vehicle. Unlike epidermal growth factor or hepatocyte growth factor (HGF), IGF-I is anabolic even in the setting of acute renal injury. These data are from the experiment described in Figure 17-16. As the data in this figure demonstrate, ARF is a highly catabolic state vehicle-treated animals experience 15 weight reduction. Animals that received IGF-I experienced only a 5 reduction in body weight and were back to baseline by 7 days. Data are expressed as mean standard error. Significant differences between groups are indicated by asterisks. (From Miller et al. 2 with permission.) Photomicrograph of kidneys from rats with acute renal failure (ARF) treated with insulin-like growth factor (IGF-I) or vehicle. These photomicrographs are of histologic sections stained with hematoxylin and eosin originating from kidneys of rats that received vehicle or IGF 1 after ischemic renal...

Metabolic Perturbations In Acute Renal Failure

Metabolic perturbations in acute renal failure (ARF). In most instances ARF is a complication of sepsis, trauma, or multiple organ failure, so it is difficult to ascribe specific metabolic alterations to ARF. Metabolic derangements will be determined by the acute uremic state plus the underlying disease process or by complications such as severe infections and organ dysfunctions and, last but not least by the type and frequency of renal replacement therapy 1, 2 .

Diagnosis Of Possible Postrenal Causes Of Acute Renal Failure

Diagnosis of possible postrenal causes of acute renal failure (ARF). Postrenal causes of ARF are less common (5 to 15 of ARF population) but are nearly always amenable to therapy. This figure depicts the historical, physical examination and tests that can lead to an intrarenal (crystal deposition) or extrarenal (blockade of the collecting system) form of obstructive uropa-thy 1, 6, 9, 10 . BUN blood urea nitrogen CT computed tomography MRI magnetic resonance imaging.

Evidence Suggesting A Role For Reactive Oxygen Metabolites In Ischemic Acute Renal Failure

Evidence suggesting a role for reactive oxygen metabolites in acute renal failure. The increased ROS production results from two major sources the conversion of hypoxanthine to xanthine by xanthine dehydrogenase and the oxidation of NADH by NADH oxi-dase(s). During the period of ischemia, oxygen deprivation results in the massive dephosphorylation of adenine nucleotides to hypox-anthine. Normally, hypoxanthine is metabolized by xanthine dehydrogenase which uses NAD+ rather than oxygen as the acceptor of electrons and does not generate free radicals. However, during ischemia, xanthine dehydrogenase is converted to xanthine oxidase. When oxygen becomes available during reperfusion, the metabolism of hypoxanthine by xanthine oxidase generates superoxide. Conversion of NAD+ to its reduced form, NADH, and the accumulation of NADH occurs during ischemia. During the reperfusion period, the conversion of NADH back to NAD+ by NADH oxidase also results in a burst of superoxide production. (From...

Acute Renal Failure Cellular Features of Injury and Repair

Although ischemic acute renal failure (ARF) is likely the result of many different factors, much tubule injury can be traced back to a number of specific lesions that occur at the cellular level in ischemic polarized epithelial cells. At the onset of an ischemic insult, rapid and dramatic biochemical changes in the cellular environment occur, most notably perturbation of the intracellular levels of ATP and free calcium and increases in the levels of free radicals, which lead to alterations in structural and functional cellular components characteristic of renal epithelial cells 1-7 . These alterations include a loss of tight junction integrity, disruption of actin-based microfilaments, and loss of the apical basolateral polarity of epithelial cells. The result is loss of normal renal cell function 7-12 .

Renal Failure Fluidallinone Solution

To ensure maximal nutrient utilization and avoid metabolic derangements as mineral imbalance, hyperglycemia or blood urea nitrogen rise, the infusion should be started at a slow rate (providing about 50 of requirements) and gradually increased over several days. Optimally, the solution should be infused continuously over 24 hours to avoid marked derangements in substrate concentrations in the presence of impaired utilization for several nutritional substrates in patients with acute renal failure. EAA, NEAA essential and nonessential amino acids TPN total parenteral nutrition.

Mortality In Acute Renal Failure Comparison Of Crrt Versus

Continuous renal replacement therapy (CRRT) versus intermittent hemodialysis (IHD) effect on mortality. Despite significant advances in the management of acute renal failure (ARF) over the last four decades, the perception is that the associated mortality has not changed significantly 26 . Recent publications suggest that there may have been some improvement during the last decade 27 . Both IHD and peritoneal dialysis (PD) were the major therapies until a decade ago, and they improved the outcome from the 100 mortality of ARF to its current level. The effect of continuous renal replacement therapy on overall patient outcome is still unclear 28 . The

Potential Causes Of Apoptosis In Acute Renal Failure

Potential causes of apoptosis in acute renal failure (ARF). The same cytotoxic stimuli that induce necrosis cause apoptosis. The mechanism of cell death induced by a specific injury depends in large part on the severity of the injury. Because most cells require constant external signals, called survival signals, to remain viable, the loss of these survival signals can trigger apoptosis. In ARF, a deficiency of growth factors and loss of cell-substrate adhesion are potential causes of apoptosis. The death pathways induced by engagement of tumour necrosis factor (TNF) with the TNF receptor or Fas with its receptor (Fas ligand) are well known causes of apoptosis in immune cells. TNF and Fas can also induce apoptosis in epithelial cells and may contribute to cell death in ARF. Therapeutic approaches, both experimental and in clinical use, to prevent and manage acute renal failure based on its pathogenetic mechanisms. ETR ET receptor GFR glomerular filtration rate HGF hepatocyte growth...

Continuous Ambulatory Peritoneal Dialysis Catheters

Peritoneal dialysis catheters are placed into the abdomen most often for continuous ambulatory peritoneal dialysis (CAPD), as well as for acute dialysis and for drainage of malignant ascites. Continuous ambulatory peritoneal dialysis offers several advantages over hemodialysis including the ability to perform dialysis without the need for vascular access, systemic heparinization, or the hemodynamic changes associated with the volume shifts of hemodialysis. In addition, the quality of life of those on CAPD may be preferred as this process can be safely completed at a patient's home, work or play, saving multiple weekly trips to a dialysis unit.

Complications Of Hemodialysis

Hypotension Excessive ultrafiltration, cardiac arrhythmia, air embolus, pericardial tamponade hemorrhage (gastrointestinal, intracranial, retroperitoneal) anaphylactoid reaction Hemolysis Inadequate removal of chloramine from dialysate, failure of dialysis of aluminum antacids Seizure Excessive urea clearance (first treatment), failure of dialysis

During peritoneal dialysis

With solutions of low glucose content (1-36 glucose) no adjustment to the normal insulin regimen is needed. Dialysates of high glucose content can however severely disrupt diabetes and additional insulin is needed. During CAPD insulin can be administered entirely from the dialysis bags soluble insulin is added to each bag, initially using the existing total daily dose in divided amounts, often giving less at night. The dose may eventually be quite different from that given subcutaneously. The technique is often satisfactory and excellent control can be achieved without hypoglycaemia. Patients whose technique is poor, and who are thus liable to peritonitis, should not be given intra-peritoneal insulin. The use of dialysis fluids with high glucose content (3-86 ), needed to alleviate fluid overload, causes havoc with diabetes control additional soluble insulin (in a dose appropriately titrated) must be given before administration of the strong glucose concentrations, or possibly more...

Management Of Recurrent Disease After Kidney Transplantation

Immunoglobulin A nephropathy Henoch-Schonlein purpura Mesangiocapillary glomerulonephritis type I Mesangiocapillary glomerulonephritis type II Membranous nephropathy Anti-glomerular basement membrane disease Hemolytic uremic syndrome Aggressive perioperative dialysis, hydration, low oxalate diet, low ascorbic acid diet, phosphate supplements, magnesium glycerophosphate, pyridoxine

Causes Of Intrinsic Acute Renal Failure

Immunoglobulins and light chains Calcium and phosphorus Uric acid and xanthine Drug-induced acute tubulointerstitial nephritis Acute pyelonephritis Tumor infiltration Radiation nephropathy Disseminated intravascular coagulation Hemolytic-uremic syndrome Malignant hypertension Vasculitis

Initiating factors and progression promoters in diabetic nephropathy

Both development and early progression of diabetic nephropathy are most likely to occur following years of poor Nephropathy initiating factors and progression diabetic control tight control over a decade both delays onset of the disease and slows progression chiefly of its early phase, although there is some effect in established disease as well. There is also a familial propensity to nephropathy in both Type 1 and Type 2 diabetes, although the precise genetic factors responsible have not been identified.

Stages of nephropathy

At the onset of Type 1 diabetes there is evidence of hyperfiltration with increased glomerular filtration rate, and large kidneys and glomeruli. These defects can be reversed by meticulous diabetic control there is however no good evidence that these changes predispose to the subsequent development of nephropathy. Stages of progression of diabetic nephropathy Stages of progression of diabetic nephropathy Course of nephropathy The natural course of diabetic nephropathy is the progression through five stages from normal renal function to end-stage renal failure as shown in the table. Incipient nephropathy, identified by the appearance of microalbuminuria, is the earliest clinical stage and is not associated with significant clinical signs or any changes other than a very small increase in blood pressure. At this stage urine testing by conventional methods will give negative or only trace positive results. As the disease progresses albuminuria increases until end-stage nephropathy, when...

Sickle Cell Nephropathy

The term sickle cell nephropathy encompasses all the structural and functional abnormalities of the kidneys seen in sickle cell disease. These renal defects are most pronounced in homozygous sickle cell anemia (Hb SS), double heterozygous sickle cell hemoglobin C disease (Hb SC), sickle cell hemoglobin D dis Speculation exists as to the possible mechanisms responsible for the decline in renal hemodynamics with age, sometimes ending in renal failure with shrunken end-stage kidneys. This decline could be the result of the loss of medullary circulation, as suggested by the microradioangiographic studies. Another possible mechanism is the relationship between supernormal hemodynamics, hyperfiltration, and glomerulosclerosis 6 . An inability to achieve maximally concentrated urine has been the most consistent feature of sickle cell nephropathy.

Categorization of Causes of Acute Renal Failure

Acute renal failure nephritis nephritis Acute renal failure (ARF). This figure depicts the most commonly used schema to classify and diagnostically approach the patient with ARF 1, 6, 9 . The most common general cause of ARF (60 to 70 of cases) is prerenal factors. Prerenal causes include those secondary to renal hypoperfusion, which occurs in the setting of extracellular fluid loss (eg, with vomiting, nasogastric suctioning, gastrointestinal hemorrhage, diarrhea, burns, heat stroke, diuretics, glucosuria), sequestration of extracellular fluid (eg, with pancreatitis,

Recommendation For Initial Dialysis Modality For Acute Renal Failure

Recommendation for initial dialysis modality for acute renal failure (ARF). Patients with multiple organ failure (MOF) and ARF can be treated with various continuous therapies or IHD. Continuous therapies provide better hemodynamic stability however, if not monitored carefully they can lead to significant volume depletion. In general, hemodynami-cally unstable, catabolic, and fluid-overloaded patients are best treated with continuous therapies, whereas IHD is better suited for patients who require early mobilization and are more stable. It is likely that the mix of modalities used will change as evidence linking the choice of modality to outcome becomes available. For now, it is probably appropriate to consider all these techniques as viable options that can be used collectively. Ideally, each patient should have an individualized approach for management of ARF.

Of Acute Renal Failure

Renal Biopsy Tools

Urinalysis in acute renal failure Pyelonephritis, interstitial nephritis Allergic interstitial nephritis, atheroemboli, glomerulopathy Urinalysis in acute renal failure (ARF). A normal urinalysis suggests a prerenal or postrenal form of ARF however, many patients with ARF of postrenal causes have some cellular elements on urinalysis. Relatively uncommon causes of ARF that usually present with oligoanuria and a normal urinalysis are mannitol toxicity and large doses of dextran infusion. In these disorders, a hyperoncotic state occurs in which glomerular capillary oncotic pressure, combined with the intratubular hydrostatic pressure, exceeds the glomerular capillary hydrostatic pressure and stop glomerular filtration. Red blood cells (RBCs) can be seen with all renal forms of ARF. When RBC casts are present, glomerulonephritis or vasculitis is most likely. White blood cells (WBCs) can also be present in small numbers in the urine of patients with ARF. Large numbers of WBCs and WBC casts...

Determinants Of Solute Removal In Dialysis Techniques For Acute Renal Failure

Determinants of solute removal in dialysis techniques for acute renal failure. Solute removal in these techniques is achieved by convection, diffusion, or a combination of these two. Convective techniques include ultrafiltration (UF) and hemofiltration (H) and they depend on solute removal by solvent drag 6 . As solute removal is solely dependent on convective clearance it can be enhanced only by increasing the volume of ultrafiltrate produced. While ultrafiltration requires fluid removal only, to prevent significant volume loss and resulting hemodynamic compromise, hemofiltration necessitates partial or total replacement of the fluid removed. Larger molecules are removed more efficiently by this process and, thus, middle molecular clearances are superior. In intermittent hemodialysis (IHD) ultrafiltration is achieved by modifying the transmembrane pressure and generally does not contribute significantly to solute removal. In peritoneal dialysis (PD) the UF depends on the osmotic...

Exogenous And Endogenous Chemicals That Cause Acute Renal Failure

Exogenous and endogenous chemicals that cause acute renal failure. Nephrotoxicants may act at different sites in the kidney, resulting in altered renal function. The sites of injury by selected nephrotoxi-cants are shown. Nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin-converting enzyme (ACE) inhibitors, cyclosporin A, and radiographic contrast media cause vasoconstriction. Gold, interferon-alpha, and penicillamine can alter glomerular function and result in proteinuria and decreased renal function. Many nephrotoxicants damage tubular epithelial cells directly. Aminoglycosides, cephaloridine, cadmium chloride, and potassium dichromate affect the S1 and S2 segments of the proximal tubule, whereas cisplatin, mercuric chloride, and dichlorovinyl-L-cysteine affect the S3 segment of the proximal tubule. Cephalosporins, cadmium chloride, and NSAIDs cause interstitial nephritis whereas phenacetin causes renal papillary necrosis. Mechanisms that contribute to decreased glomerular...

Extracellular Fluid Volume Homeostasis in Chronic Renal Failure

One Time Urine Sodium

Relation between glomerular filtration rate (GFR) and fractional sodium (Na) excretion (FENa). The normal FENa is less than 1 . Adaptations in chronic renal failure maintain urinary Na excretion equal to dietary intake until end-stage renal disease is reached. To achieve this, the FENa must increase as the GFR decreases. Effects of dietary sodium (Na) intake on extracellular fluid (ECF) volume in chronic renal failure (CRF) 75 . Compared with normal persons, patients with CRF have expanded ECF volume at normal Na intake. Furthermore, the time necessary to return to neutral balance on shifting from one to another level of Na intake is increased. Thus, whereas urinary Na excretion equals dietary intake of Na within 3 to 5 days in normal persons, this process may take up to 2 weeks in patients with CRF. This time delay means that not only are these patients susceptible to volume overload, but also to volume depletion. This phenomenon can be modeled simply by reducing the time constant...

Lithium Induced Acute Renal Failure

Acute renal failure, with or without oliguria, can be associated with lithium treatment, and with severe dehydration. In this case, acute renal failure can be considered a prerenal type consequently, it resolves rapidly with appropriate fluid therapy. Indeed, the histologic appearance in such cases is remarkable for its lack of significant abnormalities. Conditions that stimulate sodium retention and consequently lithium reabsorption, such as low salt intake and loss of body fluid by way of vomiting, diarrhea, or diuretics, decreasing lithium clearance should be avoided. With any acute illness, particularly one associated with gastrointestinal symptoms such as diarrhea, lithium blood levels should be closely monitored and the dose adjusted when necessary. Indeed, most episodes of acute lithium intoxication are largely predictable, and thus avoidable, provided that precautions are taken 25 . Removing lithium from the body as soon as possible the is...

Dialysis Modalities For Acute Renal Failure

Several methods of dialysis are available for renal replacement therapy. While most of these have been adapted from dialysis procedures developed for end-stage renal disease several variations are available specifically for ARF patients 1 . As a more continuous technique, peritoneal dialysis (PD) is an alternative for some patients. In ARF patients two forms of PD have been used. Most commonly, dialysate is infused and drained from the peritoneal cavity by gravity. More commonly a variation of the procedure for continuous ambulatory PD termed continuous equilibrated PD is utilized 4 . Dialysate is instilled and drained manually and continuously every 3 to six hours, and fluid removal is achieved by varying the concentration of dextrose in the solutions. Alternatively, the process can be automated with a cycling device programmed to deliver a predetermined volume of dialysate and drain the peritoneal cavity at fixed intervals. The cycler makes the process less labor intensive, but the...

Stepwise Approach To Diagnosis Of Acute Renal Failure

Stepwise approach to diagnosis of acute renal failure (ARF). The multiple causes, predisposing factors, and clinical settings demand a logical, sequential approach to each case of ARF. This figure presents a four-step approach to assessing ARF patients in an effort to delineate the cause in a timely and cost-effective manner. Step 1 involves a focused history, record review, and examination. The salient features of these analyses are noted in more detail in Figure 12-13. In many cases, a single bladder catheterization is needed to assess the degree of residual volume, which should be less than 30 to 50 mL. Urinalysis is a critical part of the initial evaluation of all patients with ARF. Generally, a relatively normal urinalysis suggests either a prerenal or postrenal cause, whereas a urinalysis containing cells and casts is most compatible with a renal cause. A detailed schema of urinalysis interpretation in the setting of ARF is depicted in Figure 12-15. Usually, after Step 1 the...

Metabolic Alterations in Acute Renal Failure

Energy metabolism in acute renal failure (ARF). In experimental animals ARF decreases oxygen consumption even when hypothermia and acidosis are corrected (uremic hypometabolism) 3 . In contrast, in the clinical setting oxygen consumption of patients with various form of renal failure is remarkably little changed 4 . In subjects with chronic renal failure (CRF), advanced uremia (UA), patients on regular hemodialysis therapy (HD) but also in patients with uncomplicated ARF (ARFNS) resting energy expenditure (REE) was comparable to that seen in controls (N). However, in patients with ARF and sepsis (ARFS) REE is increased by approximately 20 .

Epidemiology of Acute Renal Failure

EPIDEMIOLOGY OF ACUTE RENAL FAILURE Prospective studies. Prospective epidemiologic studies of acute renal failure (ARF) in large populations have not often been published . The first study reported by Eliahou and colleagues 4 was developed in Israel in the 1960s and included only Jewish patients. This summary of available data suggests a progressive increase in ARF incidence that at present seems to have stabilized around 200 cases per million population per year (pmp y). No data about ARF incidence are available from undeveloped countries. EPIDEMIOLOGY OF ACUTE RENAL FAILURE NEED OF DIALYSIS European Dialysis and Number of patients needing dialysis for acute renal failure (ARF), expressed as cases per million population per year (pmp y). This has been another way of assessing the incidence of the most severe cases of ARF. Local situations, mainly economics, have an effect on dialysis facilities for ARF management. In 1973 Israeli figures showed a lower rate of dialysis than other...

Actions Of Growth Factors In Acute Renal Failure

Difference Between Arf And Crf

Selected actions of growth factors in the setting of acute renal failure (ARF). After an acute renal injury, a spectrum of molecular responses occur involving the local expression of growth factors and their receptors. In addition, there is considerable variation in the mechanisms by which the growth factors are beneficial for ARF. After an Rationale for the use of insulin-like growth factor IGF-I in the setting of acute renal failure (ARF). Of the growth factors that have been demonstrated to improve outcomes after acute renal injury, the most progress has been made with IGF-I. From this table, it is evident that IGF-I has a broad spectrum of activities, which makes it a logical choice for treatment of ARF. An agent that increased renal plasma flow and glomerular filtration rate and was mito-genic for proximal tubule cells and anabolic would address several features of ARF. Serial serum creatinine values in rats with ischemic acute renal failure (ARF) treated with insulin-like growth...

Indications And Timing Of Dialysis For Acute Renal Failure Renal Replacement Versus Renal Support

Timing of intervention Indications for dialysis Dialysis dose Dialysis intervention in acute renal failure (ARF) renal replacement versus renal support. An important consideration in the management of ARF is defining the goals of therapy. Several issues must be considered, including the timing of the intervention, the amount and frequency of dialysis, and the duration of therapy. In practice, these issues are based on individual preferences and experience, and no immutable criteria are followed 7,23 . Dialysis intervention in ARF is usually considered when there is clinical evidence of uremia symptoms or biochemical evidence of solute and fluid imbalance. An important consideration in this regard is to recognize that the patient with ARF is somewhat different than the one with endstage renal disease (ESRD). The rapid decline of renal function associated with multiorgan failure does not permit much of an adaptive response which characterizes the course of the patient with ESRD. As a...

Causes Of Parenchymatous Acute Renal Failure

Acute tubular necrosis Hemodynamic cardiovascular surgery,* sepsis,* prerenal causes* Toxic antimicrobials,* iodide contrast agents,* anesthesics, immunosuppressive or antineoplastic agents,* Chinese herbs, Opiaceous, Extasis, mercurials, organic solvents, venoms, heavy metals, mannitol, radiation Intratubular deposits acute uric acid nephropathy, myeloma, severe hypercalcemia, Acute tubulointerstitial nephritis (see Fig. 8-4) thrombosis or embolism, bilateral renal vein thrombosis Small vessels atheroembolic disease, thrombotic microangiopathy, hemolytic-uremic syndrome or thrombotic thrombocytopenic purpura, postpartum acute renal failure, antiphospholipid syndrome, disseminated intravascular coagulation, scleroderma, malignant arterial hypertension, radiation nephritis, vasculitis endocarditis, or shunt Henoch-Schonlein purpura Essential mixed cryoglobulinemia Systemic lupus erythematosus ImmunoglobulinA nephropathy Mesangiocapillary

Causes Of Electrolyte Derangements In Acute Renal Failure

Renal Failure Degree

Electrolytes in acute renal failure (ARF) causes of hyperkalemia and hyperphosphatemia. ARF frequently is associated with hyper-kalemia and hyperphosphatemia. Causes are not only impaired renal excretion of electrolytes but release during catabolism, altered distribution in intracellular and extracellular spaces, impaired cellular uptake, and acidosis. Thus, the type of underlying disease and degree of hypercatabolism also determine the occurrence and severity of electrolyte abnormalities. Either hypophosphatemia or hyperphosphatemia can predispose to the development and maintenance of ARF 37 . Electrolytes in acute renal failure (ARF) hypophosphatemia and hypokalemia. It must be noted that a considerable number of patients with ARF do not present with hyperkalemia or hyperphos-phatemia, but at least 5 have low serum potassium and more than 12 have decreased plasma phosphate on admission 38 . Nutritional support, especially parenteral nutrition with low electrolyte content, can cause...

Contributing Factors To Protein Catabolism In Acute Renal Failure

Renal Failure Degree

Protein catabolism in acute renal failure (ARF) contributing factors. The causes of hypercatabolism in ARF are complex and multifold and present a combination of nonspecific mechanisms induced by the acute disease process and underlying illness and associated complications, specific effects induced by the acute loss of renal function, and, finally, the type and intensity of renal replacement therapy. Amino acid pools and amino acid utilization in acute renal failure (ARF). As a consequence of these metabolic alterations, imbalances in amino acid pools in plasma and in the intracellular compartment occur in ARF. A typical plasma amino acid pattern is seen 16 . Plasma concentrations of cysteine (CYS), taurine (TAU), methionine (MET), and phenylalanine (PHE) are elevated, whereas plasma levels of valine (VAL) and leucine (LEU) are decreased. Metabolic functions of the kidney and protein and amino acid metabolism in acute renal failure (ARF). Protein and amino acid metabolism in ARF are...

Comparison Of Dialysis Prescription And Dose Delivered In Crrt And

Dialysis Prescription Dialysis Dose Delivered Comparison of dialysis prescription and dose delivered in continuous renal replacement (CRRT) and intermittent hemodialysis (IHD). The ability of each modality to achieve a particular clearance is influenced by the dialysis prescription and the operational characteristics however, it must be recognized that there may be a significant difference between the dialysis dose prescribed and that delivered. In general, IHD techniques are limited by available time, and in catabolic patients it may not be possible to achieve a desired level of solute control even by maximizing the operational characteristics.

Feckless patient with endstage renal failure

A 44-year-old woman with type 1 diabetes of 26 years' duration, proliferative retinopathy, profound neuropathy and end-stage renal failure treated by renal transplant had her feet checked at monthly intervals at the renal unit as part of a research protocol. Her foot pulses were palpable. She was educated in foot care, foot inspections and early reporting of any problems. However, during a 3-year period she suffered nine separate episodes of foot trauma, none of which she reported early they were detected at Fig. 6.10 This patch of necrosis developed on the apex of the 1st toe of a patient in end-stage renal failure treated by renal transplantation. Her pedal pulses were palpable. The patch of necrosis began as a small crack in the nail sulcus and spread very slowly to involve most of the toe, which was amputated because of severe pain. She smoked 25 cigarettes a day. Fig. 6.11 This patient in end-stage renal failure treated with renal transplantation dropped an object on her toe and...

Amino Acid Solutions For The Treatment Of Acute Renal Failure Nephro Solutions

Amino acid (AA) solutions for parenteral nutrition in acute renal failure (ARF). The most controversial choice regards the type of amino acid solution to be used either essential amino acids (EAAs) exclusively, solutions of EAA plus nonessential amino acids (NEAAs), or specially designed nephro solutions of different proportions of EAA and specific NEAA that might become conditionally essential for ARF (see Fig. 18-11). Use of solutions of EAA alone is based on principles established for treating chronic renal failure (CRF) with a low-protein diet and an EAA supplement. This may be inappropriate as the metabolic adaptations to low-protein diets in response to CRF may not have occurred in patients with ARF. Plus, there are fundamental differences in the goals of nutritional therapy in the two groups of patients, and consequently, infusion solutions of EAA may be sub-optimal. tions or in special proportions designed to counteract the metabolic changes of renal failure (nephro...

Relationship Between The Clinical And Cellular Phases Of Ischemic Acute Renal Failure

Relationship between the clinical and cellular phases of ischemic acute renal failure. Prerenal azotemia results from reduced renal blood flow and is associated with reduced organ function (decreased glomerular filtration rate), but cellular integrity is maintained through vascular and cellular adaptive responses. The initiation phase occurs when renal blood flow decreases to a level that results in severe cellular ATP depletion that, in turn, leads to acute cell injury. Severe cellular ATP depletion causes a constellation of cellular alterations culminating in proximal tubule cell injury, cell death, and organ dysfunction 2 . During the clinical phase known as maintenance, cells undergo repair, migration, apoptosis, and proliferation in an attempt to re-establish and maintain cell and tubule integrity 3 . This cellular repair and reorganization phase results in slowly improving cell and organ function. During the recovery phase, cell differentiation continues, cells mature, and...

Causes of Acute Renal Failure

Characteristics of acute renal failure. Acute renal failure is a syndrome characterized by a sudden decrease of the glomerular filtration rate (GFR) and consequently an increase in blood nitrogen products (blood urea nitrogen and creatinine). It is associated with oliguria in about two thirds of cases. Depending on the localization or the nature of the renal insult, ARF is classified as prerenal, parenchymatous, or obstructive (postrenal). CAUSES OF PRERENAL ACUTE RENAL FAILURE Causes of prerenal acute renal failure (ARF). Prerenal ARF, also known as prerenal uremia, supervenes when glomerular filtration rate falls as a consequence of decreased effective renal blood supply. The condition is reversible if the underlying disease is resolved. CAUSES OF PARENCHYMATOUS ACUTE RENAL FAILURE Acute tubular necrosis Hemodynamic cardiovascular surgery,* sepsis,* prerenal causes* Toxic antimicrobials,* iodide contrast agents,* anesthesics, immunosuppressive or antineoplastic agents,* Chinese...

Decisions For Nutrition In Patients With Acute Renal Failure

What patient with acute renal failure needs nutritional support 3. At what degree of impairment in renal function should the nutritional regimen be adapted for renal failure Nutrition in patients with acute renal failure (ARF) decision making. Not every patient with ARF requires nutritional support. It is important to identify those who will benefit and to define the optimal time to initiate therapy 1 . The nutritional regimen should be adapted for renal failure when renal function is impaired. The multiple metabolic alterations characteristic of ARF occur when kidney function is below 30 of normal. Thus, when creatinine clearance falls below 50 to 30 mL per minute 1.73 m2 (or serum creatinine rises above 2.5 to 3.0 mg dL) the nutritional regimen should be adapted to ARF. With the exception of severe hepatic failure and massively deranged amino acid metabolism (hyperammonemia) or protein synthesis (depletion of coagulation factors) renal failure is the major determinant of the...

Renovascular Hypertension and Ischemic Nephropathy

The major issues in approaching patients with renal artery stenosis relate to the role of renal artery stenosis in the management of hypertension, ie, renovascular hypertension, and to the potential for vascular compromise of renal function, ie, ischemic nephropathy. Ever since the original Goldblatt experiment in 1934, wherein experimental hypertension was produced by renal artery clamping, countless investigators and clinicians have been intrigued by the relationship between renal artery stenosis and hypertension. Much discussion has focused on the pathophysiology of renovascular hypertension, the renin angiotensin system, diagnostic tests to detect presumed renovascular hypertension, and the relative merits of surgical renal revascularization (SR), percutaneous transluminal renal angioplasty (PTRA), and drug therapy in managing patients with renal artery stenosis and hypertension. Hemodynamically significant renal artery stenosis, when bilateral or affecting the artery to a...

Diagnosis Of Possible Pigmentassociated Forms Of Acute Renal Failure

Diagnosis of possible pigment-associated forms of acute renal failure (ARF). Once prerenal and postrenal forms of ARF have been ruled out and renal vascular, glomerular, and interstitial processes seem unlikely, a diagnosis of acute tubular necrosis (ATN) is probable. A diagnosis of ATN is thus one of exclusion (of other causes of ARF). In the majority of cases when ATN is present, one or more of the three predisposing conditions have been identified to be operational. These conditions include renal ischemia due to a prolonged prerenal state, nephrotoxin exposure, and sometimes pigmenturia. A diagnosis Nephrotoxin acute renal failure (ARF). A variety of nephrotoxins have been implicated in causing 20 to 30 of all cases of ARF. These potential nephrotoxins can act through a variety of mechanisms to induce renal dysfunction 6, 20, 21 . CEI converting enzyme inhibitor NSAID nonsteroidal anti-inflammatory drugs.

Prophylaxis And Treatment Of Acute Uric Acid Nephropathy And Acute Tumor Lysis Syndrome

Correct initial electrolyte and fluid imbalance, and azotemia, if possible dialysis as indicated for established renal failure or unresponsive electrolyte or metabolic abnormalities C. Patients presenting (usually after chemotherapy) with renal failure 1. Same as for patients with tumor and hyperuricemia if sufficient renal function remains. If dialysis is necessary, continuous hemodialysis or hemofiltration may be preferable if severe hyperuricemia or hyperkalemia is present

Vascular Causes Of Acute Renal Failure

Vascular causes of acute renal failure (ARF). Once prerenal and postrenal causes of ARF have been excluded, attention should be focused on the kidney. One useful means of classifying renal causes of ARF is to consider the anatomic compartments of the kidney. Thus, disorders of the renal vasculature (see Fig. 12-18), glomerulus (see Fig. 12-19), interstitium (see Fig. 12-20) and tubules can all result in identical clinical pictures of ARF 1 . This figure depicts the disorders of the renal arterial and venous systems that can result in ARF 15 .


Diabetic nephropathy is the kidney disease that occurs as a result of diabetes and is also a sign of worsening blood vessels throughout the body. It is a leading cause of end-stage renal disease in Europe and the USA. Albumin, a large blood protein, is an early marker for development of nephropathy in patients with type II diabetes. As nephropathy starts to develop, there is a progressive leak of large protein molecules from the kidneys into the urine. It has been observed that patients who progress from microalbuminuria (albumin creatinine ratio 3-299 g mg_1) to macroalbuminuria (albumin creatinine ratio > 300 g mg_1) are likely to progress to end-stage renal failure 28 . Healthy blood glucose levels have shown to delay the onset of microalbu-minuria and the progression of microalbuminuria into macroalbuminuria in patients with type II diabetes 22 . Strategies for slowing the progression of diabetic nephropathy include managing hypertension 29 , optimizing glycaemic control 14 ,...

Acute Renal Failure

Nephrotoxic may account for approximately 50 of all cases of acute and chronic renal failure. Nephrotoxic renal injury often occurs in conjunction with ischemic acute renal failure. Acute renal failure may occur in 2 to 5 of hospitalized patients and 10 to 15 of patients in intensive care units. The mortality of acute renal failure is approximatley 50 which has not changed significantly in the last 40 years.

Renal Failure

Approximately 70 of patients with FHF secondary to acetaminophen toxicity have renal failure compared with 30 of patient with FHF of other causes. Renal insufficiency may result from prerenal azotemia, acute tubular necrosis (ATN), or functional renal failure (hepatorenal syndrome). Determination of urine sodium concentration may be useful in distinguishing ATN from these other possibilities and measurement of central venous pressure or pulmonary capillary wedge pressure can be used to exclude prerenal azotemia. Continuous venovenous hemodialysis is the preferred means of renal support in the setting of FHF. Intermittent dialysis should be avoided as it may result in hypotension and exacerbate intracranial hypertension.

Diabetic nephropathy

The development of proteinuria in any diabetic patient is ominous. It is associated with a risk of severe retinopathy and neuropathy, and above all carries a major increased risk in mortality from coronary artery disease, as well as progression to renal failure in some patients. Yet developments in this field to improve the prognosis have been substantial. The overall prevalence of proteinuria in Type 1 diabetes has decreased over half a century from more than 50 of patients down to between 10 and 20 , presumably as a result of better overall diabetic care. Furthermore, at the earliest sign of proteinuria, administration of medication and very tight blood pressure control ameliorate the course of the disease and substantially delay the development of renal failure. And for those who are less fortunate, transplantation and dialysis restore a good quality of life to the majority. Cumulative incidence of nephropathy in patients diagnosed with Type 1 diabetes over a 20-year span...


Lipid peroxidation is increased during haemodialysis, because ofROS generation 188-190 , Paradoxically, total antioxidant capacity increases in patients undergoing dialysis due to high serum urate levels, although this decreases after dialysis, as does serum ATC 189 , Increased ROS generation has also been reported to increase apoptosis in leukocytes 191 . Potentially, this offers the interesting possibility of using either treatment of dialysis membranes with ATC


Phrosis was the most common problem identified in the renal tract by Ratan and colleagues, but in other series the rate is between 2 and 10 41 . In most series hydronephrosis is used to refer to a uretero-pelvic junction impairment to urine flow. The management of these patients has not been specifically discussed the general approach is prophylactic antibiotics and observation, with approximately 25 requiring surgical reconstruction 14 . Surgical reconstruction is needed in those patients with an increasing hydro-nephrosis, deteriorating renal function, or symptoms 14 .

Causes Of Volume Expansioncauses Of Volume Depletion

Inherited hypertension (Liddle's syndrome, glucocorticoid remediable hyperaldosteronism, pseudohypoaldosteronism Type II, others) Renal failure Diuretic phase of oliguric acute renal failure Postobstructive diuresis Nonoliguric acute renal failure Salt-wasting nephropathy Medullary cystic disease Tubulointerstitial disease Nephrocalcinosis

Epidemiology Pathology And Taxonomy Geographical distribution

Bacterial kidney disease is commonly observed in cultured salmonid stocks from North America, continental Europe, Japan (Fryer and Sanders, 1981), South America (Sanders and Barros, 1986), Scotland (Bruno, 1986c) and Scandinavia (Ljungberg et al., 1990 Gudmundsdottir et al., 1993). Significant populations of free-ranging fish also harbour R. salmoninarum (Pippy, 1969 Evelyn et al., 1973 Ellis et al., 1978 Mitchum et al., 1979 Paterson et al, 1979, 1981b Banner et al., 1986 Souter et al., 1986 Elliott and Pascho, 1991 Sanders et al., 1992, Meyers et al., 1993).

Malignancy In The Renal Transplant Patient

B-cell lymphoproliferative syndromes (Epstein-Barr virus) Kaposi's sarcoma Cutaneous form Visceral and cutaneous form Genitourinary cancer Carcinoma of the native kidney (acquired cystic kidney disease) Carcinoma of the transplanted kidney Renal cell carcinoma Malignant melanoma Carcinoma of the urinary bladder (cyclophosphamide associated) Uroepithelial tumors (associated with analgesic abuse) Gynecologic cancer Carcinoma of the cervix Ovarian cancer

Medical Complications of Renal Transplantation

Medical complications in the renal allograft recipient represent the often overlapping impact of several variables. At the time of transplantation, significant comorbidity may already be present and can be of immediate concern. Other problems may have originated in the milieu of chronic renal failure, such as hyperparathyroid bone disease or hypertension, but may evolve differently after transplantation. Finally, new complications may result from specific toxicities of pharmaceutical agents, reflecting the overall impact of immunosuppression. In many cases, all of these elements contribute to overt clinical illness. For instance, cardiovascular disease is now the most common cause of death in renal allograft recipients 1 . Coronary disease may have predated transplantation (indeed, coronary disease is a common cause of death among all patients with end-stage renal disease). After transplantation, hypertension and hyperlipidemia, perhaps exacerbated by administration of cyclosporine...

Selected Bibliography

Morris GC Jr, DeBakey ME, Cooley MJ Surgical treatment of renal failure of renovascular origin. JAMA 1962, 182 113-116. Mailloux LU, Napolitano B, Bellucci AG, et al. Renal vascular disease causing end-stage renal disease, incidence, clinical correlates, and outcomes a 20-year clinical experience. Am J Kidney Dis 1994, 24 622-639. Hansen KJ, Thomason RB, Craven TE, et al. Surgical management of dialysis-dependent ischemic nephropathy. J Vasc Surg 1995, 21 197-209. Textor SC, McKusick MA, Schirger AA, et al. Atherosclerotic renovascular disease in patients with renal failure. Adv Nephrol Necker Hosp 1997, 27 281-295. Harden PN, MacLeod MJ, Rodger RSC, et al. Effect of renal-artery stenting on progression of renovascular renal failure. Lancet 1997, 349 1133-1136.

Correlation Of Steadystate Serum Creatinine Concentration And Glomerular Filtration Rate

Renal Failure History of kidney disease, hypertension, abnormal urinalysis Categories of renal failure. Once the presence of renal failure is ascertained by elevated blood urea nitrogen (BUN) or serum creati-nine value, the clinician must decide whether it is acute or chronic. When previous values are available for review, this judgment is made relatively easily. In the absence of such values, the factors depicted here may be helpful. Hemoglobin potentially undergoes nonenzymatic carbamylation of its terminal valine 8 . Thus, similar to the hemoglobin A1C value as an index of blood sugar control, the level of carbamylated hemoglobin is an indicator of the degree and duration of elevated BUN, but, this test is not yet widely available. The presence of small kidneys strongly suggests that renal failure is at least in part chronic. From a practical standpoint, because even chronic renal failure often is partially reversible, the clinician should assume and evaluate for the presence of...

Therapeutic Trials Of Insulinlike Growth Factor I In Humans

Summary of an abstract describing the trial of insulin-like growth factor (IGF-I) in the treatment of patients with established acute renal failure (ARF). Based on the accumulated animal and human data, a multicenter, double-blind, randomized, placebo-controlled trial was performed to examine the effects of IGF-I in patients with established ARF. Enrolled patients had ARF of a wide variety of causes, including surgery, trauma, hypertension, sepsis, and nephro-toxic injury. Approximately 75 patients were enrolled, treatment being initiated within 6 days of the renal insult. Renal function was evaluated by iodothalimate clearance. Unfortunately, at an interim analysis (the study was originally designed to enroll 150 patients) there was no difference in renal function or survival between the groups. The investigators recognized several potential problems with the trial, including the severity of many patients' illnesses, the variety of causes of the renal injury, and delay in initiating...

Arthur H Cohen Richard J Glassock

The primary glomerulopathies are those disorders that affect glomerular structure, function, or both in the absence of a multisystem disorder. The clinical manifestations are predominately the consequence of the glomerular lesion (such as proteinuria, hematuria, and reduced glomerular filtration rate). The combination of clinical manifestations leads to a variety of clinical syndromes. These syndromes include acute glomerulomphritis rapidly progressive glomerulonephritis chronic renal failure the nephrotic syndrome or asymptomatic hematuria, proteinuria, or both.

Lack Of Effect Of Recombinant

Limitations in the use of growth factors to treat acute renal failure (ARF). The disappointing results of several recent clinical trials of ARF therapy reflect the fact that our understanding of its pathophysiology is still limited. Screening compounds using animal models may be irrelevant. Most laboratories use relatively young animals, even though ARF frequently affects older humans, whose organ regenerative capacity may be limited. In addition, our laboratory models are usually based on a single insult, whereas many of our patients suffer repeated or multiple insults. Until we gain a better understanding of the basic pathogenic mechanisms of ARF, studies in human patients are likely to be frustrating.

Estimation Of Energy Requirements

Energy requirements of patients with acute renal failure (ARF) have been grossly overestimated in the past and energy intakes of more than 50 kcal kg of body weight (BW) per day (ie, about 100 above resting energy expenditure (REE) haven been advocated 6 . Adverse effects of overfeeding have been extensively documented during the last decades, and it should be noted that energy intake must not exceed the actual energy consumption. Energy requirements can be calculated with sufficient accuracy by standard formulas such as the Harris Benedict equation. Calculated REE should be multiplied with a stress factor to correct for hypermetabolic disease however, even in hypercatabolic conditions such as sepsis or multiple organ dysfunction syndrome, energy requirements rarely exceed 1.3 times calculated REE 1 . Protein metabolism in acute renal failure (ARF) activation of protein catabolism. Protein synthesis and degradation rates in acutely uremic and...

Lorraine C Racusen Cynthia C Nast

Causes of acute renal failure can be divided into three categories 1) prerenal, due to inadequate perfusion 2) postrenal, due to obstruction of outflow and 3) intrinsic, due to injury to renal parenchyma. Among the latter, diseases of, or injury to, glomeruli, vessels, interstitium, or tubules may lead to a decrease in glomerular filtration rate (GFR). Glomerular diseases that lead to acute renal failure are the proliferative glomerulonephritides, including postinfectious and membranoprolif-erative glomerulonephritis secondary to glomerular deposition of immune complexes. If glomerular injury is severe enough to damage the glomerular basement membrane, leakage of fibrin and other plasma proteins stimulates formation of cellular extracapillary crescents composed of epithelial cells and monocytes and macrophages. Crescents may form as a result of an inflammatory reaction to immune complexes formed to nonglomerular antigens antibody reaction to intrinsic glomerular antigens, as in...

Richard E Rieselbach A Vishnu Moorthy Marc B Garnick

Patients with malignancy are particularly vulnerable to development of renal abnormalities 1 . Additionally, patients with renal abnormalities who have undergone kidney transplantation are at increased risk for malignancy, which may involve the kidney 2 . Malignancy may directly involve the urinary tract. More commonly, however, the many systemic manifestations of cancer and the toxicity of its treatment are involved in the pathogenesis of diverse clinical syndromes involving the kidney 3 . Finally, a high percentage of cancer patients are candidates for aggressive chemotherapy or radiation therapy, or both. Nephrotoxicity due to chemotherapy may manifest as acute renal failure, chronic renal failure, or specific tubular dysfunction causing fluid and electrolyte imbalance 7 . The nephrotoxicity of radiation therapy may be synergistic with that of chemotherapy in some settings, or radiation therapy may by itself produce significant renal damage.

Hospital Related Epidemiologic Data

Acute renal failure initial hospital location and mortality. A, Initial departmental location of ARF patients in a hospital in a Western country. The majority of the cases initially were seen in medical, surgical, and intensive care units (ICUs). The cases initially treated in nephrology departments were community acquired, whereas the ARF patients in the other settings generally acquired ARF in those settings. Obstetric-gynecologic ARF cases have almost disappeared. ARF of traumatic origin is also rare, for Acute Renal Failure in Hospitalized Patients (per 1000 admissions) Epidemiologic variable. The incidence of hospital-acquired acute renal failure (ARF) depends on what epidemiologic method is used. In case-control studies the incidence varied between 49 and 19 per thousand. When the real occurrence was measured in large populations over longer intervals, the incidence of hospital-acquired ARF decreased to 1.5 per thousand admissions. (Data from 1,5,16,17,18 .)

Nutrition Renal Function and Recovery

A, B, Impact of nutritional interventions on renal function and course of acute renal failure (ARF). Starvation accelerates protein breakdown and impairs protein synthesis in the kidney, whereas refeeding exerts the opposite effects 49 . In experimental animals, provision of amino acids or total parenteral nutrition accelerates tissue repair and recovery of renal function 50 . In patients, however, this has been much more difficult to prove, and only one study has reported on a positive effect of TPN on the resolution of ARF 51 . Impact of nutritional interventions on renal function in acute renal failure (ARF). Amino acid infused before or during ischemia or nephrotoxicity may enhance tubule damage and accelerate loss of renal function in rat models of ARF. In part, this therapeutic paradox 53 from amino acid alimentation in ARF is related to the increase in metabolic work for transport processes when oxygen supply is limited, which may aggravate ischemic injury 54 . Similar...

Michael S Goligorsky Wilfred Lieberthal

Acute renal failure (ARF) is a syndrome characterized by an abrupt and reversible kidney dysfunction. The spectrum of inciting factors is broad from ischemic and nephrotoxic agents to a variety of endotoxemic states and syndrome of multiple organ failure. The pathophysiology of ARF includes vascular, glomerular and tubular dysfunction which, depending on the actual offending stimulus, vary in the severity and time of appearance. Hemodynamic compromise prevails in cases when noxious stimuli are related to hypotension and septicemia, leading to renal hypoperfusion with secondary tubular changes (described in Chapter 13). Nephrotoxic offenders usually result in primary tubular epithelial cell injury, though endothelial cell dysfunction can also occur, leading to the eventual cessation of glomerular filtration. This latter effect is a consequence of the combined action of tubular obstruction and activation of tubuloglomerular feedback mechanism. In the following pages we shall review the...

Contrast Medium Associated Nephrotoxicity

RISK FACTORS THAT PREDISPOSE TO CONTRAST ASSOCIATED NEPHROPATHY Chronic renal failure Diabetic nephropathy nephropathy Risk factors that predispose to contrast-associated nephropathy. In random populations undergoing radiocontrast imaging the incidence of contrasts associated nephropathy defined by a change in serum creatinine of more than 0.5 mg dL or a greater than 50 increase over baseline, is between 2 and 7 . For confirmed high-risk patients (baseline serum creatinine values greater than 1.5 mg dL) it rises to 10 to 35 . In addition, there are suspected risk factors that should be taken into consideration when considering the value of contrast-enhanced imaging. Contrast associated nephropathy els, a consensus is developing to the effect that contrast-associated nephropathy involves combined toxic and hypoxic insults to the kidney 35 . The initial glomerular vasoconstriction that follows the injection of radiocontrast medium induces the liberation of both vasoconstrictor...

Risk Factors For Renal Involvement In Dysproteinemias

Acute deterioration of renal function (5-10 ) Dehydration Hypercalcemia Cast nephropathy Crescentic glomerulonephritis Chronic renal insufficiency (45-75 ) Myeloma cast nephropathy Light chain (AL) amyloidosis Interstitial plasma cell infiltration (rare) Proteinuria-nephrotic syndrome (50-80 ) Light chain (AL) amyloidosis Light chain deposition disease Heavy chain deposition disease Cryoglobulinemic glomerular lesions Fanconi's syndrome (1 ) Secondary lesions (20-30 ) Pyelonephritis Nephrocalcinosis Hyperuricemic nephropathy Factors enhancing amyloid formation Unfolding of paraprotein X Light chain Factors enhancing cast nephropathy High urinary excretion of light chains Binding of light chain to Tamm-Horsfall protein (THP) Iso-electric point of light chain > 5.1 (enhances binding to anionic THP (pI 3.2) Tendency to self-aggregation of light chains k Light chain Presence of hydrophobic aminoacids in CDR1 or CDR2 of VL-chain Deletion of CH1 domain Fc part immunoglobulin Factors...

Brian G Dwinnell Robert J Anderson

Acute renal failure (ARF) is abrupt deterioration of renal function sufficient to result in failure of urinary elimination of nitrogenous waste products (urea nitrogen and creatinine). This deterioration of renal function results in elevations of blood urea nitrogen and serum creatinine concentrations. While there is no disagreement about the general definition of ARF, there are substantial differences in diagnostic criteria various clinicians use to define ARF (eg, magnitude of rise of serum creatinine concentration). From a clinical perspective, for persons with normal renal function and serum creatinine concentration, glomerular filtration rate must be dramatically reduced to result in even modest increments (eg, 0.1 to 0.3 mg dL) in serum creatinine concentration. Moreover, several studies demonstrate a direct relationship between the magnitude of serum creatinine increase and mortality from ARF. Thus, the clinician must carefully evaluate all cases of rising serum creatinine.

Bruce A Molitoris Robert Bacallao

Ischemia remains the major cause of acute renal failure (ARF) in the adult population 1 . Clinically a reduction in glomerular filtration rate (GFR) secondary to reduced renal blood flow can reflect prerenal azotemia or acute tubular necrosis (ATN). More appropriate terms for ATN are acute tubular dysfunction or acute tubular injury, as necrosis only rarely is seen in renal biopsies, and renal tubular cell injury is the hallmark of this process. Furthermore, the reduction in GFR during acute tubular dysfunction can now, in large part, be related to tubular cell injury. Ischemic ARF resulting in acute tubular dysfunction secondary to cell injury is divided into initiation, maintenance, and recovery phases. Recent studies now allow a direct connection to be drawn between these clinical phases and the cellular phases of ischemic ARF (Fig. 13-1). Thus, renal function can be directly related to the cycle of cell injury and recovery.

Rick G Schnellmann Katrina J Kelly

Humans are exposed intentionally and unintentionally to a variety of diverse chemicals that harm the kidney. As the list of drugs, natural products, industrial chemicals and environmental pollutants that cause nephrotoxicity has increased, it has become clear that chemicals with very diverse chemical structures produce nephrotoxicity. For example, the heavy metal HgCl2, the myco-toxin fumonisin B1, the immunosuppresant cyclosporin A, and the aminoglycoside antibiotics all produce acute renal failure but are not structurally related. Thus, it is not surprising that the cellular targets within the kidney and the mechanisms of cellular injury vary with different toxicants. Nevertheless, there are similarities between chemical-induced acute tubular injury and ischemia reperfusion injury.

Overview Of Blood Urea Nitrogen And Serum Creatinine

Overview of blood urea nitrogen (BUN) and serum creatinine. Given the central role of BUN and serum creatinine in determining the presence of renal failure, an understanding of the metabolism of these substances is needed. Urea nitrogen derives from the breakdown of proteins that are delivered to the liver. Thus, the urea nitrogen production rate

Steven B Miller Babu J Padanilam

The kidney possesses a remarkable capacity for restoring its structure and functional ability following an ischemic or toxic insult. It is unique as a solid organ in its ability to suffer an injury of such magnitude that the organ can fail for weeks and yet recover full function. Studying the natural regenerative process after an acute renal insult has provided new insights into the pathogenesis of acute renal failure (ARF) and possible new therapies. These therapies may limit the extent of injury or even accelerate the regenerative process and improve outcomes for patients suffering with ARF. In this chapter we illustrate some of the molecular responses of the kidney to an acute insult and demonstrate the effects of therapy with growth factors in the setting of experimental models of ARF. We conclude by demonstrating strategies that will provide future insights into the molecular response of the kidney to injury.

Giuseppe DAmico Franco Ferrario

The clinical picture varies during the long-term course of the disease, being characterized by periods of temporary reactivation (nephritic or nephrotic syndrome, sometimes with rapidly occurring renal insufficiency) and long-lasting periods of partial remission. Only infrequently does end-stage renal failure develop however, mortality as a result of the other complications of the systemic disease (mainly cardiovascular) is rather frequent.

Garabed Eknoyan Luan D Truong

As a rule, diseases of the kidney primarily affect the glomeruli, vasculature, or remainder of the renal parenchyma that consists of the tubules and interstitium. Although the interstitium and the tubules represent separate functional and structural compartments, they are intimately related. Injury initially involving either one of them inevitably results in damage to the other. Hence the term tubulointerstitial diseases is used. Because inflammatory cellular infiltrates of variable severity are a constant feature of this entity, the terms tubulointerstitial diseases and tubulointerstitial nephritis have come to be used interchangeably. The clinicopathologic syndrome that results from these lesions, commonly termed tubulointerstitial nephropathy, may pursue an acute or chronic course. The chronic course is discussed here. The abbreviation TIN is used to refer synonymously to chronic tubulointer-stitial nephritis and tubulointerstitial nephropathy. TIN may be classified as primary or...

Treatment Of Hemodynamic Instability

Exclude nondialysis-related causes (eg, cardiac ischemia, pericardial effusion, infection) Set the dry weight accurately Optimize the dialysate composition Use a sodium concentration of > 140 mEq L Use sodium modeling Use a bicarbonate buffer Avoid low magnesium dialysate Avoid low calcium dialysate Optimize the method of ultrafiltration Use volume-controlled ultrafiltration Use ultrafiltration modeling Use sequential ultrafiltration and isovolemic dialysis Use cool temperature dialysate Maximize cardiac performance Have patients avoid food on day of dialysis Have patients avoid antihypertensive medicines on day of dialysis Pharmacologic prevention Erythropoietin therapy to keep hematocrit > 30 Experimental (eg,caffeine, midodrine, ephedrine, phenylephrine, carnitine)

Ramesh Khanna Karl D Nolph

Peritoneal dialysis is a technique whereby infusion of dialysis solution into the peritoneal cavity is followed by a variable dwell time and subsequent drainage. Continuous ambulatory peritoneal dialysis (CAPD) is a continuous treatment consisting of four to five 2-L dialysis exchanges per day (Fig. 4-1A). Diurnal exchanges last 4 to 6 hours, and the nocturnal exchange remains in the peritoneal cavity for 6 to 8 hours. Continuous cyclic peritoneal dialysis, in reality, is a continuous treatment carried out with an automated cycler machine (Fig. 4-1B). Multiple short-dwell exchanges are performed at night with the aid of an automated cycler machine. Other peritoneal dialysis treatments consist of intermittent regimens (Fig. 4-2A-C). During peritoneal dialysis, solutes and fluids are exchanged between the capillary blood and the intraperitoneal fluid through a biologic membrane, the peritoneum. The three-layered peritoneal membrane consists of 1) the mesothelium, a continuous monolayer...

TK Sreepada Rao David Roth

Infection with hepatitis B virus (HBV) may be associated with a variety of renal diseases. In the past, HBV was the major cause of viral hepatitis in patients with end-stage renal disease (ESRD). Introduction of rigorous infection-control strategies has led to a remarkable decline in the spread of HBV infection in dialysis units. Physicians also are increasingly recognizing the association between chronic hepatitis C virus (HCV) infection and glomerular disease, both in native kidneys and renal allografts. Liver disease caused by HCV is a major factor in morbidity and mortality among patients with ESRD treated with dialysis and transplantation. The first part of this chapter focuses mainly on issues related to HCV infection. The second part of this chapter examines the renal complications in patients with human immunodeficiency virus (HIV) infection.

Robert A Kyle Morie A Gertz

In primary amyloidosis (AL) the fibrils consist of the variable portions of monoclonal (k) or (X) immunoglobulin light chains or, very rarely, heavy chains. In secondary amyloidosis (AA) the fibrils consist of protein A, a non-immunoglobulin. In familial amyloidosis (AF) the fibrils are composed of mutant transthyretin (prealbumin) or, rarely, fibrinogen or apolipoprotein. In senile systemic amyloidosis the fibrils consist of normal transthyretin. The amyloid fibrils associated with long-term dialysis (A M dialysis arthropathy) consist of -microglobulin.

Common Causes Of Malignant Hypertension

Primary (essential) malignant hypertension* Secondary malignant hypertension Primary renal disease Chronic glomerulonephritis* Chronic pyelonephritis* Analgesic nephropathy* Immunoglobulin A nephropathy* Acute glomerulonephritis Radiation nephritis Renovascular hypertension* Oral contraceptives

Plasma Cell Dyscrasias

The arrow indicates a multinucleated giant cell. B, Light chain deposition disease. Note the changes indicative of chronic TIN and light chain deposition along the tubular basement membrane (dark purple). C, Immunofluorescent stain for k light chain deposition along the tubular basement membrane. The renal complications of multiple myeloma are a major risk factor in the morbidity and mortality of this neoplastic disorder. Whereas the pathogenesis of renal involvement is multifactorial (hypercal-cemia and hyperuricemia), it is the lesions that result from the excessive production of light chains that cause chronic TIN. These lesions are initiated by the precipitation of the light chain dimers in the distal tubules and result in what has been termed myeloma cast nephropathy. The affected tubules are surrounded by multinucleated giant cells. Adjoining tubules show varying degrees of atrophy. The propensity of light chains to lead to myeloma cast nephropathy...

Histology of Renal Lesions in Dysproteinemias

In about 60 of patients with this renal lesion, nodular expansion of the mesangium is seen that resembles nodular diabetic nephropathy 75,76 . The nodules stained purple with periodic acid-Schiff (PAS) stain have a homogeneous appearance, and those stained with methenamine silver are pink-brownish in color. In a few cases, a more mesangiocapillary pattern of injury is present. The tubular basement membranes (TBMs) are

Mechanisms of Extracellular Fluid Volume Expansion in Nephrotic Syndrome

Time course of recovery from minimal change nephrotic syndrome in five children. Note that urinary Na excretion (squares) increases before serum albumin concentration increases. The data suggest that the natriuresis reflects a change in intrinsic renal Na retention. The data also emphasize that factors other than hypoalbuminemia must contribute to the Na retention that occurs in nephrosis. UNaV urinary Na excretion volume. (Data from Oliver and Owings 70 .)

Other Conditions That Recur In Renal Allografts

Differentiation from acute and chronic vascular rejection can be difficult Renal transplantation does not halt the progress of Fabry's disease because the new kidney is not an adequate source of a-galactosidase patients have frequent systemic complications Nephrosis reported between 21 and 60 mo

John D Pirsch Jon S Odorico Hans W Sollinger

In the United States, diabetes mellitus is the third most common disease and fourth leading cause of death from disease. Diabetes is the leading cause of blindness, the number one cause of amputations and impotence, and one of the most frequently occurring chronic childhood diseases. Diabetes is also the leading cause of end-stage renal disease in the United States, with a prevalence rate of 31 compared with other renal diseases. Diabetes is also the most frequent indication for kidney transplantation, accounting for 22 of all transplantation operations. Increasingly, pancreas transplantation is being offered to patients who would benefit from kidney transplantation (called simultaneous pancreas-kidney transplantation) or who have had a previously successful kidney transplantation (called sequential pancreas after kidney transplantation). Relatively few transplantation centers are performing pancreas transplantation alone in patients with severe life-threatening complications of...

Antigenic crossreactivity

Of this technique are that it is still three- to fourfold less sensitive than the monoclonal-based ELISA and, secondly, even if antigen is confirmed, the presence of viable organisms is still in question. Therefore, it is recommended that, if putative R. salmoninarum-free stocks are identified as ELISA-positive, Western blot and culture techniques be used to confirm the presence of p57 and viable R. salmoninarum. Using this type of combined approach for detecting R. salmoninarum, Griffiths et al. (1996) have found that incubation of ovarian fluid cellular debris in selective kidney disease medium (SKDM) broth, followed by Western blotting, increased the total numbers of positive samples by 32 over SKDM agar culture or indirect FAT (IFAT).

Hyperkalemia Diagnostic Approach

Hyporeninemic Hypoaldosteronism

Either leukocytes or platelets results in leakage of potassium from these cells. Familial pseudohyperkalemia is a rare condition of increased potassium efflux from red blood cells in vitro. Ischemia due to tight or prolonged tourniquet application or fist clenching increases serum potassium concentrations by as much as 1.0 to 1.6 mEq L. Hyperkalemia can also result from decreases in K movement into cells or increases in potassium movement from cells. Hyper-chloremic metabolic acidosis (in contrast to organic acid, anion-gap metabolic acidosis) causes potassium ions to flow out of cells. Hypertonic states induced by mannitol, hypertonic saline, or poor blood sugar control promote movement of water and potassium out of cells. Depolarizing muscle relaxants such as succinylcholine increase permeability of muscle cells and should be avoided by hyperkalemic patients. The mechanism of hyperkalemia with -adrenergic blockade is illustrated in Figure 3-3. Digitalis impairs function of the...

Renal Handling of Magnesium

Glomerulus Filtration Physiology

Tion of Mg and about 20 of the filtered Mg has been reabsorbed. Mg reabsorption occurs passively through paracellular pathways. Hydrated Mg has a very large radius that decreases its intercellular permeability in the PCT when compared with sodium. The smaller hydrated radius of sodium is 50 to 60 reabsorbed in the PCT. No clear evidence exists of transcellular reabsorption or secretion of Mg within the mammalian PCT. In the pars recta of the proximal straight tubule (PST), Mg reabsorption can continue to occur by way of passive forces in the concentrating kidney. In states of normal hydration, however, very little Mg reabsorption occurs in the PST. Within the thin descending limb of the loop of Henle, juxtamedullary nephrons are capable of a small amount of Mg reabsorption in a state of antidiuresis or Mg depletion. This reabsorption does not occur in superficial cortical nephrons. No data exist regarding Mg reabsorption in the thin ascending limb of the loop of Henle. No Mg...

Composition Of Replacement Fluid And Dialysate For Crrt

Composition of dialysate and replacement fluids used for continuous renal replacement therapy (CRRT). One of the key features of any dialysis method is the manipulation of metabolic balance. In general, this is achieved by altering composition of dialysate or replacement fluid . Most commercially available dialysate and replacement solutions have lactate as the base however, bicarbonate-based solutions are being utilized more and more 17,18 .

Lance D Dworkin Douglas G Shemin

Hypertension is a cause and consequence of chronic renal disease. Data from the United States Renal Data System (USRDS) identifies systemic hypertension as the second most common cause of end-stage renal disease, with diabetes mellitus being the first. Renal failure in patients with hypertension has many causes, including functional impairment secondary to vascular disease and hypertensive nephrosclerosis. Even in those in whom hypertension is not the primary process damaging the kidney, elevations in systemic blood pressure may accelerate the rate at which kidney function is lost. This accelerated loss of kidney function occurs particularly in patients with glomerular diseases and clinically evident proteinuria. Hypertension may damage the kidney by several mechanisms. Because autoregulation of glomerular pressure is impaired in chronic renal disease, elevations in systemic blood pressure also are associated with increased glomerular capillary pressure. Glomerular hypertension...

Operational Characteristics

Trisodium Citrate Mechanism Crrt

Anticoagulation in Dialysis for ARF Anticoagulation in Dialysis for ARF Factors influencing dialysis-related thrombogenicity. One of the major determinants of the efficacy of any dialysis procedure in acute renal failure (ARF) is the ability to maintain a functioning extracorporeal circuit. Anticoagulation becomes a key component in this regard and requires a balance between an appropriate level of anticoagulation to maintain patency of the circuit and prevention of complications. Figures 19-4 and 19-5 show the mechanisms of thrombus formation in an extracorporeal circuit and the interaction of various factors in this process. (From Ward 9 with permission.) Modalities for anticoagulation for continuous renal replacement therapy. While systemic heparin is the anticoagulant most commonly used for dialysis, other modalities are available. The utilization of these modalities is largely influenced by prevailing local experience. Schematic diagrams for heparin, A, and citrate, B,...

Growth Factor Production

Hgf Cmet Myelin

Production of epidermal growth factor (EGF), insulin-like growth factor (IGF-I), and hepatocyte growth factor (HGF) by various tissues. EGF, IGF-I, and HGF have all been demonstrated to improve outcomes in various animal models of acute renal failure (ARF). All three growth-promoting factors are produced in the kidneys and in a variety of other organs. The local production is probably most important for recovery from an acute renal insult. The influence of production in other organs in the setting of ARF has yet to be determined. This chapter deals primarily with local production and actions of EGF, IGF-I, and HGF. Receptor binding for epidermal growth factor (EGF). EGF binding in kidney under basal conditions is extensive. The most significant specific binding occurs in the proximal convoluted (PCT) and proximal straight tubules. There is also significant EGF binding in the glomeruli (GLOM), distal convoluted tubules (DCT), and the entire collecting duct (OMCD, IMCD). After an...

Blood Urea Nitrogen Buncreatinine Ratio

The blood urea nitrogen (BUN)-creatinine ratio. Based on the information in Figure 12-3, the BUN-creatinine ratio often deviates from the usual value of about 10 1. These deviations may have modest diagnostic implications. As an example, for reasons as yet unclear, tubular reabsorption of urea nitrogen is enhanced in low-urine flow states. Thus, a high BUN-creatinine ratio often occurs in prerenal and postrenal (see Fig. 12-6) forms of renal failure. Similarly, enhanced delivery of amino acids to the liver (as with catabolism, corticosteroids, etc.) can enhance urea nitrogen formation and increase the BUN-creatinine ratio. A BUN-creatinine ratio lower than 10 1 can occur because of decreased urea nitrogen formation (eg, in protein malnutrition, advanced liver disease), enhanced creatinine formation (eg, with rhabdomyolysis), impaired tubular secretion of creatinine (eg, secondary to trimethoprim, cimetidine), or relatively enhanced removal of the small substance urea nitrogen by...

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