Natural Remedies for Kidney Stones
A renal calculus25 (kidney stone) is a hard granule of calcium, phosphate, uric acid, and protein. Renal calculi form in the renal pelvis and are usually small enough to pass unnoticed in the urine flow. Some, however, grow to several centimeters in size and block the renal pelvis or ureter, which can lead to the destruction of nephrons as pressure builds in the kidney. A large, jagged calculus passing down the ureter stimulates strong contractions that can be excruciatingly painful. It can also damage the ureter and cause hematuria. Causes of renal calculi include hypercalcemia, dehydration, pH imbalances, frequent urinary tract infections, or an enlarged prostate gland causing urine retention. Calculi are sometimes treated with stone-dissolving drugs, but often they require surgical removal. A nonsurgical technique called lithotripsy26 uses ultrasound to pulverize the calculi into fine granules easily passed in the urine.
Normally, dietary oxalate (and bile acids) is bound to calcium in the intestinal tract. This renders oxalate unavailable for absorption. However, when significant steatorrhea is present, unabsorbed fatty acids preferentially bind to calcium, the free oxalate enters the colon and is absorbed. The absorbed oxalate is then filtered by the kidneys where it becomes free to bind calcium with the potential for kidney stone formation. Foods such as chocolate, tea, cola, spinach, celery, and carrots should be avoided, as should dehydration. Although some of the vitamin C in the TPN solutions may be converted to oxalate with a resultant hyperoxaluria, patients without a colon do not appear at increased risk for oxalate nephrolithiasis.
Stones refer to hypercalcemia-induced nephrolithiasis, seen in 30 to 60 of cases of primary hyperparathyroidism. In parathyroid carcinoma, it is not uncommon to see both nephrolithiasis (kidney stones) and nephrocalcinosis (precipitation of calcium phosphate in the renal tubules). Untreated and unmanaged, both complications may lead to irreversible azotemia and renal failure. One recent study revealed a prevalence of renal insufficiency of 84 in parathyroid carcinoma.8 In addition, hypercalcemia leads to an obligatory calciuria with large-volume polyuria that can result in significant intravascular volume depletion, further contributing to the underlying azotemia.
Amino acid transport in the proximal tubule. Cystinuria is the leading single gene cause of inheritable urolithiasis in both children and adults 41,42 . Three Mendelian disorders, Dent's disease, X-linked recessive nephrolithiasis, and X-linked recessive hypophospha-temic rickets cause hypercalciuric urolithiasis. These disorders involve a functional loss of the renal chloride channel ClC-5 43 . The common molecular basis for these three inherited kidney stone diseases has led to speculation that ClC-5 also may be involved in other renal tubular disorders associated with kidney stones. Hereditary renal hypour-icemia is an inborn error of renal tubular transport that appears to involve urate reabsorption in the proximal tubule 16 .
Proteinuria, hypertension, or kidney stones in living prospective donors. Prospective donors with pyuria must be evaluated for possible infection and other reversible abnormalities. Proteinuria is generally a contraindication to donation. Hypertension also must be considered at least a relative contraindication to donation. Patients with a history of nephrolithiasis but no current or recent stones may be considered for donation after first undergoing urologic and metabolic evaluations for stones. (From Kasiske and coworkers 2 with permission.)
Excess weight shortens life expectancy and increases a person's risk of atherosclerosis, hypertension, diabetes mellitus, joint pain and degeneration, kidney stones, and gallstones cancer of the breast, uterus, and liver in women and cancer of the colon, rectum, and prostate gland in men. The excess thoracic fat in obese people interferes with breathing and results in increased blood Pco2, sleepiness, and reduced vitality. Obesity is also a significant obstacle to successful surgery.
Medullary sponge kidney (MSK) diagnosed by intravenous urography in 53-year-old woman with a history of recurrent kidney stones. Pseudocystic collections of contrast medium in the papillary areas (arrows) are the typical feature of MSK. They result from congenital dilatation of collecting ducts (involving part or all of one or both kidneys), ranging from mild ectasia (appearing on urography as linear striations in the papillae, or papillary blush ) to frank cystic pools, as in this case (giving a spongelike appearance on section of the kidney). MSK has an estimated prevalence of 1 in 5000 2 . It predisposes to stone formation in the dilated ducts on plain films, clustering of calcifications in the papillary areas is very suggestive of the condition. MSK may be associated with a variety of other congenital and inherited disorders, including corporeal hemihypertrophy, Beckwith-Wiedemann syndrome (macroglossia, omphalocele, visceromegaly, microcephaly, and mental retardation), polycystic...
Uric acid contributes to the risk of kidney stones in several ways. Pure uric acid stones occur in patients with hyperuricosuria, particularly when the urine is acidic. Thus, therapy involves both allopurinol and alkalinization with potassium alkali salts. Hyperuricosuria also promotes calcium oxalate stone formation. In these patients, calcium nephrolithiasis can be prevented by therapy with allopurinol. The mechanism may involve heterogenous nucleation of calcium oxalate by uric acid microcrystals, binding of endogenous inhibitors of calcium crystallization, or salting out of calcium oxalate by urate 4 .
Patients with SBS not only have an inadequate absorptive surface but also have an increased intestinal transit time. These patients have an elevated serum gastrin level and the excess gastric acid that is produced exacerbates the diarrhea (1,8). The mechanism for the hypergastrinemia is not known and this state is usually transient (1,8). In addition, the loss of brush border hydrolases causes inadequate carbohydrate breakdown, contributing to osmotic diarrhea. If the terminal ileum has been resected, bile acids are not well absorbed, which results in sodium and water secretion in the colon, again adding to diarrhea. Loss of the bile acid pool will cause steatorrhea and malabsorption of fat-soluble vitamins (A, D, E, and K). This disruption of the enterohepatic circulation of bile can lead to both cholesterol gallstones and oxalate kidney stones.
Nephrocalcinosis in type I (distal) renal tubular acidosis. Nephrocalcinosis and nephrolithiasis are common complications in distal renal tubular acidosis (RTA-1). Several factors contribute to the pathogenesis. The most important of these factors are a reduction in urinary excretion of citrate and a persistently alkaline urine. Citrate inhibits the growth of calcium stones its excretion is reduced in RTA-1 as a result of
51 Tips for Dealing with Kidney Stones
Do you have kidney stones? Do you think you do, but aren’t sure? Do you get them often, and need some preventative advice? 51 Tips for Dealing with Kidney Stones can help.