Causes of Acute Renal Failure

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Sudden causes Induce Called affecting

Sudden causes Induce Called affecting

FIGURE 8-1

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

Decreased effective extracellular volume

Renal losses: hemorrhage, vomiting, diarrhea, burns, diuretics

Redistribution: hepatopathy, nephrotic syndrome, intestinal obstruction, pancreatitis, peritonitis, malnutrition Decreased cardiac output: cardiogenic shock, valvulopathy, myocarditis, myocardial infarction, arrhythmia, congestive heart failure, pulmonary emboli, cardiac tamponade Peripheral vasodilation: hypotension, sepsis, hypoxemia, anaphylactic shock, treatment with interleukin L2 or interferons, ovarian hyperstimulation syndrome Renal vasoconstriction: prostaglandin synthesis inhibition, a-adrenergics, sepsis, hepatorenal syndrome, hypercalcemia Efferent arteriole vasodilation: converting-enzyme inhibitors

FIGURE 8-2

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 herbs, Opiaceous, Extasis, mercurials, organic solvents, venoms, heavy metals, mannitol, radiation Intratubular deposits: acute uric acid nephropathy, myeloma, severe hypercalcemia, primary oxalosis, sulfadiazine, fluoride anesthesics Organic pigments (endogenous nephrotoxins): Myoglobin rhabdomyolisis: muscle trauma; infections; dermatopolymyositis; metabolic alterations; hyperosmolar coma; diabetic ketoacidosis; severe hypokalemia; hyper- or hyponatremia; hypophosphatemia; severe hypothy-roidism; malignant hyperthermia; toxins such as ethylene glycol, carbon monoxide, mercurial chloride, stings; drugs such as fibrates, statins, opioids and amphetamines; hereditary diseases such as muscular dystrophy, metabolopathies, McArdle disease and carnitine deficit Hemoglobinuria: malaria; mechanical destruction of erythrocytes with extracorporeal circulation or metallic prosthesis, transfusion reactions, or other hemolysis; heat stroke; burns; glucose-6-phosphate dehydrogenase; nocturnal paroxystic hemoglobinuria; chemicals such as aniline, quinine, glycerol, benzene, phenol, hydralazine; insect venoms

Acute tubulointerstitial nephritis (see Fig. 8-4)

Vascular occlusion

Principal vessels: bilateral (unilateral in solitary functioning kidney) renal artery 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

Acute glomerulonephritis Postinfectious: streptococcal or other pathogen associated with visceral abscess, endocarditis, or shunt Henoch-Schonlein purpura Essential mixed cryoglobulinemia Systemic lupus erythematosus ImmunoglobulinA nephropathy Mesangiocapillary

With antiglomerular basement membrane antibodies with lung disease

(Goodpasture is syndrome) or without it Idiopathic, rapidly progressive, without immune deposits

Cortical necrosis, abruptio placentae, septic abortion, disseminated intravascular coagulation

FIGURE 8-3

Causes of parenchymal acute renal failure (ARF). When the sudden decrease in glomerular filtration rate that characterizes ARF is secondary to intrinsic renal damage mainly affecting tubules, interstitium, glomeruli and/or vessels, we are facing a parenchymatous ARF. Multiple causes have been described, some of them constituting the most frequent ones are marked with an asterisk.

MOST FREQUENT CAUSES OF ACUTE TUBULOINTERSTITIAL NEPHRITIS

CAUSES OF OBSTRUCTIVE ACUTE RENAL FAILURE

Antimicrobials

Immunological

Penicillin

Systemic lupus erythematosus

Ampicillin

Rejection

Rifampicin

Infections (at present quite rare)

Sulfonamides

Neoplasia

Analgesics, anti-inflammatories

Myeloma

Fenoprofen

Lymphoma

Ibuprofen

Acute leukemia

Naproxen

Idiopathic

Amidopyrine

Isolated

Glafenine

Associated with uveitis

Other drugs

Cimetidine

Allopurinol

Most common causes of tubulointerstitial nephritis. During the last years, acute tubulointerstitial nephritis is increasing in importance as a cause of acute renal failure. For decades infections were the most important cause. At present, antimicrobials and other drugs are the most common causes.

Congenital anomalies

Retroperitoneal fibrosis

Infections

Ureterocele

Idiopathic

Schistosomiasis

Bladder diverticula

Poctorinr i irothriïl

Associated with anrtir anoi irvcm

Tuberculosis i .anriiriiacic

rUolCIIUI Ul CU liai valu Go

Neurogenic bladder

a Ul LIU al ICUI Vol 11

Aspergillosis

Acquired uropathies

Iatrogenic

Actinomycosis

Benign prostatic hypertrophy

Drug-induced

Other

Urolithiasis

Gynecologic non-neoplastic

Accidental urethral

Papillary necrosis

Pregnancy-related

catheter occlusion

Iatrogenic ureteral ligation

Uterine prolapse

Malignant diseases

Endometriosis

Prostate

Acute uric acid nephropathy

Bladder

Drugs

Urethra

e-Aminocaproic acid

Cervix

Sulfonamides

Colon

Breast (metastasis)

Causes of obstructive acute renal failure. Obstruction at any level of the urinary tract frequently leads to acute renal failure. These are the most frequent causes.

\ 2.5% /

Other parenchymal 4.5%

ATN

ATN

A/ATIN

43.1% /

/'''V, Other parenchymal / 6.4%

^—Arterial disease

Prerenal

3.4%

Prerenal

Obstructive \10% /

40.6%

21%

Acute-on-chronic 13%

n = 202

n = 748

A

1977-1980

B

1991

This figure shows a comparison of the percentages of the different types of acute renal failure (ARF) in a western European country in 1977-1980 and 1991: A, distribution in a typical Madrid hospital; B, the Madrid ARF Study [1]. There are two main differences: 1) the appearance of a new group in 1991, "acute on chronic ARF," in which only mild forms (serum creatinine concentrations between 1.5 and 3.0 mg/dL) were considered, for methodological reasons; 2) the decrease in prerenal ARF suggests improved medical care. This low rate of prerenal ARF has been observed by other workers in an intensive care setting [2]. The other types of ARF remain unchanged.

Condition

Incidence (per million persons per year)

95% CI

Acute tubular necrosis

88

79-

97

Prerenal acute renal failure

46

40-

52

Acute on chronic renal failure

29

24-

-34

Obstructive acute renal failure

23

19-

27

Glomerulonephritis (primary or secondary)

6.3

4.8-

8.3

Acute tubulointerstitial nephritis

3.5

1.7-

5.3

Vasculitis

3.5

1.7-

5.3

Other vascular acute renal failure

2.1

0.8-

3.4

Total

209

195-

223

FINDINGS OF THE MADRID STUDY

FIGURE 8-7

Incidences of different forms of acute renal failure (ARF) in the Madrid ARF Study [1]. Figures express cases per million persons per year with 95% confidence intervals (CI).

Nursing School Hsp Nephritis

Sclerodermal crisis 1 Tumoral obstruction 1 Secondary glomerulonephritis 1 Vasculitis 1

Malignant hypertension 2.1 Myeloma 2.1

Acute tubulointerstitial nephritis 2.1 Atheroembolic disease 4.2

FIGURE 8-8

The most frequent causes of acute renal failure (ARF) in patients with preexisting chronic renal failure are acute tubular necrosis (ATN) and prerenal failure. The distribution of causes of ARF in these patients is similar to that observed in patients without previous kidney diseases. (Data from Liano et al. [1])

Bun/SCr increase

Previous SCr increased and/or

Normal or big kidneys (excluding amiloidosis and polycystic kidney disease and/or t SCr > 0.5 mg/dL/d and/or

Previous SCr normal

Flare of previous disease

Acute-on-chronic renal failure r

Echography

Urinary tract dilatation

Normal

Repeat echograph after 24 h

Normal

Parenchymatous glomerular or systemic ARF

Data indicating glomerular or systemic disease?

Yes

Vascular ARF

Great or small vessel disease?

Improvement with specific treatment?

Acute tubulointerstitial nephritis

Data indicating interstitial disease?

Prerenal ARF

Tumor lysis Sulfonamides Amyloidosis Other

Crystals or tubular deposits?

Acute tubular necrosis

FIGURE 8-9

Discovering the cause of acute renal failure (ARF). This is a great challenge for clinicians. This algorithm could help to determine the cause of the increase in blood urea nitrogen (BUN) or serum creatinine (SCr) in a given patient.

BIOPSY RESULTS IN THE MADRID STUDY

Disease

Patients, n

Primary GN

12

Extracapillary

e

Acute proliferative

3

Endocapillary and extracapillary

2

Focal sclerosing

1

Secondary GN

e

Antiglomerular basement membrane

3

Acute postinfectious

2

Diffuse proliferative (systemic lupus erythematosus)

1*

Vasculitis

10

Necrotizing

s*

Wegener's granulomatosis

3

Not specified

2

Acute tubular necrosis

4*

Acute tubulointerstitial nephritis

4

Atheroembolic disease

2

Kidney myeloma

2*

Cortical necrosis

1

Malignant hypertension

1

ImmunoglobulinA GN + ATN

1

Hemolytic-uremic syndrome

1

Not recorded

2

* One patient with acute-on-chronic renal failure.

FIGURE 8-10

Biopsy results in the Madrid acute renal failure (ARF) study. Kidney biopsy has had fluctuating roles in the diagnostic work-up of ARF. After extrarenal causes of ARF are excluded, the most common cause is acute tubular necrosis (ATN). Patients with well-established clinical and laboratory features of ATN receive no benefit from renal biopsy. This histologic tool should be reserved for parenchymatous ARF cases when there is no improvement of renal function after 3 weeks' evolution of ARF. By that time, most cases of ATN have resolved, so other causes could be influencing the poor evolution. Biopsy is mandatory when a potentially treatable cause is suspected, such as vasculitis, systemic disease, or glomerulonephritis (GN) in adults. Some types of parenchymatous non-ATN ARF might have histologic confirmation; however kidney biopsy is not strictly necessary in cases with an adequate clinical diagnosis such as myeloma, uric acid nephropathy, or some types of acute tubulointerstitial nephritis . Other parenchymatous forms of ARF can be accurately diagnosed without a kidney biopsy. This is true of acute post-strepto-coccal GN and of hemolytic-uremic syndrome in children. Kidney biopsy was performed in only one of every 16 ARF cases in the Madrid ARF Study [1]. All patients with primary GN, 90% with vasculitis and 50% with secondary GN were diagnosed by biopsy at the time of ARF. As many as 15 patients were diagnosed as having acute tubulointerstitial nephritis, but only four (27%) were biopsied. Only four of 337 patients with ATN (1.2%) underwent biopsy. (Data from Liano et al. [1].)

* One patient with acute-on-chronic renal failure.

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