Renal stone disease

Idiopathic hypercalciuria, a common cause of renal stone disease, may be reduced by thiazide diuretics... 

Bihl G, Meyers A 2001 Recurrent renal stone disease — advances in pathogenesis and clinical management. Lancet 358 651-656 Brater D C 1998 Diuretic therapy. New England Journal of Medicine 339 387-395 Dumont L, Mardirosoff C, Tramer MR 2000 Efficacy and harm of pharmacological prevention of acute mountain sickness quantitative review. British Medical Journal 321 267-272 Hackett P H, Roach R C 2001 High-altitude sickness. 

Henderson MJ. Renal stone disease Investigative aspects. Arch Dis Child 1993 68 160-2. 

Henderson MJ. Stone analysis is not useful in the routine investigation of renal stone disease. Ann CHn Biochem 1995 32 109-11. 

Jaeger P. Genetic versus environmental factors in renal stone disease. Curr Opin Nephrol Hyperten 1996 5 342-6. 

The amount of calcium excreted into the urine reflects intestinal absorption, skeletal resorption, and renal tubular filtration and reabsorption. Under fasting conditions, the intestinal and renal components are relatively fixed, and calcium excretion (miUigrams per 100 mL of GF) in the fasting state is used to assess the skeletal component. A value exceeding 0.16 mg/lOO mL (>0.04 mmol/L) of GF usually implies an increase in osteoclastic bone resorption. This test is useftil in assessing renal stone disease and high-turnover osteoporosis. 

Renal effects of hypercalcemia include reduced glomerular filtration rate (GFR), polyuria, nephrocalcinosis, and renal stone disease. Hypercalcemia causes renal vasoconstriction which may contribute to decreased GFR. The hypercalcemia-induced polyuria results from 1) an impairment of active transport of NaCl in the loop of Henle, distal tubule and collecting duct and 2) an inhibition of vasopressin-facilitated absorption of water in the distal nephron. As a direct result of the polyuria, many side effects including polydipsia, thirst, nocturia and dehydration are common. Precipitation of calcium salts within the kidney leads to chronic inflammatory reactions (nephrocalcinosis), fibrosis, renal impairment, nephrolithiasis and urolithiasis. Further renal damage may occur indirectly from hypertension. 

Williams, H. E. "Metabolic Aspects of Renal Stone Disease. 1975-1976. The Year in Metabolism", Ed. Freinkel, N., Plenum... 

Computer-Directed Chelate Therapy of Renal Stone Disease Martin Rubin and Arthur E. Martell... 

Carlson CA, Gravenstein JS, Gravenstein N. Ventricular tachycardia during ESWL etiology, treatment, and prevention. In Gravenstein JS, Peter K, eds. Extracorporeal Shock Wave Lithotripsy for renal stone disease Technical and clinical aspects. Boston Butterworth, 1986 119-123. 

Whatever treatment is chosen for renal stone disease, ultrasonography and plain radiography are used to monitor outcome. 

Rice bran fiber has fructo-oligosaccharides - a pre-biotic that helps friendly bacteria to proliferate in the gastrointestinal environment and improves intestinal and colon health (Tomlin and Read, 1988). Recent studies in humans (Kahlon and Chow, 1997) have revealed that rice bran fiber not only normalizes bowel function, but also helps in conditions such as irritable bowel syndrome (IBS), inflammatory bowel disease (IBD) and Crohn s disease, and lowers the lipid levels. Rice bran fiber has been shown to significantly reduce renal stones (Jahnen et al., 1992). It is a good source of fiber in weight loss programs and therapeutic fiber diets for diabetics and heart patients. Fiber diets prevent cancer of the colon and large bowel, control obesity and improve bowel function. 

Other papers in the Symposium deal with the antioxidant and hypolipidemic effects of IP6, its chelating effects in heavy metal toxicity, inhibition of renal stones and other beneficial effects such as inhibition of platelet aggregation, inhibition of inflammatory responses (Shamsuddin, 1998). The lipid lowering effect and anti-neoplastic effect of 1P6 were extensively reviewed (Jariwalla, 1999). Hence, 1P6 is a valuable component of rice bran in preventing disease and maintaining health. 1P6 is present at 1.8-2% in rice bran. 

Mis-localisation of annexin 2 has recently been implicated in the pathogenesis of Dent s disease. This term is now used collectively to describe what was previously four conditions that affect kidney function X-linked recessive nephrolithiasis with renal failure, X-linked recessive hypophosphatemic rickets, idiopathic low molecular weight proteinuria with hypercalciuria and nephrocalcinosis and Dent s disease. Patients with this condition present with low molecular weight proteinuria and hypercalciuria. Renal stones, nephrocalcinosis and renal failure are common late-stage developments. The condition has been attributed to abnormal acidification within endosomes of the proximal tubular cells. It is very rare and is usually caused by mutations in the voltage-dependent Cl /H+ chloride antiporter CLCN5, but occasionally in the PI4,5P2 5-phosphatase, OCRL1 (oculocerebrorenal syndrome of Lowe protein 1). 

Kidneys Dysfunction of the proximal tubule may occur as a late manifestation of Wilson s disease. Epithelial flattening, a loss of the brush-border membrane, mitochondrial anomalies and fatty cellular changes can be observed. These findings are, in turn, responsible for proteinuria with a predominance of hyperaminoaciduria (L. UzMAN et al., 1948). Enhanced calciuria and phosphat-uria may cause osteomalacia as well as hypoparathyroidism. (329, 344) Glucosuria and uricosuria, if present, are without clinical relevance. Due to decreased bicarbonate resorption, tubular acidosis may occur, with a tendency towards osteomalacia as well as the development of nephrocalcinosis and renal stones (in some 15% of cases). (344, 356, 392) The intensity of the copper deposits in the kidneys correlates closely with the cellular changes and functional disorders. The glomerular function is not compromised, with the result that substances normally excreted in the urine are not retained. 

Evidence for renal oxalate toxicity was found from studies describing urinary enzyme excretion suggesting renal (tubular) damage in patients with stones [25]. Rat models of stone disease have been used to study such damage in greater detail and revealed brush border loss, release of cellular enzymes, and epithelial erosion [19, 26, 27]. However, all these arguments are indirect and cannot distinguish oxalate (or oxalic acid) mediated effects from calcium oxalate crystal induced effects. 

Cao LC, Jonassen Ja, Honeyman T, Scheid C. Oxalate-induced redistribution of phosphatidylserine in renal epithelial cells implications for kidney stone disease. Am.J.Nephrol 2001 21 (69) 77. 

Scheid C, Cao LC, Honeyman T, Jonassen Ja. How elevated oxalate can promote kidney stone disease changes at the surface and in the cytosol of renal cells that promote crystal adherence and growth. Frontiers in Bioscience 2004 1(9) 797-808. 

De Swart PM JR, Busemann Sokole E, Wilmink JM. The interrelationship of calcium and magnesium absorption in idiopathic hypercalciuria and renal calcium stone disease. J Urol 1998 159 669-72. 

Cystinuria is a disorder of renal and gastrointestinal tract amino acid transport that also affects lysine, ornithine, and arginine. The four amino acids share a common transport mechanism (discussed above). Clinically, it presents as urinary stone disease because of the insolubility of cystine. In cystinosis, cystine crystals are deposited in tissues because of a transport defect in ATP-dependent cystine efflux from lysosomes (discussed above). 

Systemic complications of Crohn s disease are common, and similar to those found with ulcerative colitis. Arthritis, iritis, skin lesions, and liver disease often accompany Crohn s disease. Renal stones occur in up to 10% of patients with Crohn s disease (less frequently with ulcerative colitis) and are caused by fat malabsorption, which allows for greater oxalate absorption and formation of calcium oxalate stones. Gallstones also occur with greater frequency in patients with ileitis, possibly because of bile acid malabsorption at the terminal ileum. 

Hyperparathyroidism results from oversecretion of PTH. This condition leads to excessive bone turnover and demineralization and must be treated by removal of the parathyroid gland. The disorder is classified into primary, secondary, and tertiary hyperparathyroidism. Sporadic primary hyperparathyroidism is the third most common endocrine disorder, after diabetes and hyperthyroidism. It is most common in females older than 55 years of age and the leading cause is a single adenoma, which secretes the hormone constitu-tively, without regulation. Symptoms can include osteopenia and bone fractures, renal stones resulting from hypercalciuria, peptic ulcer disease, and pancreatitis. In milder cases, patients are asymptomatic or suffer only muscle weakness, fatigue, and/or depression. 

The occurrence of renal stone formation might well date back to early man. The oldest urolith ever recovered, from an Egyptian grave, has been estimated as 6000 years old. Although stone formation seems to have been common during medieval times, surgical treatment, performed by the stone cutters, was difficult if not deadly. Bladder stone formation, as opposed to upper urinary tract stone formation, appears to have been the dominant form of disease during ancient times the last century has seen a shift in dominance. 

Chronic cadmium toxicity occurs in industrial workers exposed to cadmium fumes. The symptoms are those of nephrotoxicity, bone disease and. to a lesser extent, hepatotoxicity. Renal stone formation may be increased. 

Uric acid nephrolithiasis calcium renal stones Malignant mesothelioma Status epilepticus Herpes simplex encephalitis Neurosyphilis Status epilepticus Cognitive dysfunction Malignant non-Hodgkin s lymphomas Treatment of PCP associated with AIDS Acanthamoeba keratitis Peripheral arterial occlusive disease Congenital or acquired protein C deficiency Respiratory distress syndrome associated with prematurity... 

The frequency of hyperuricosuria, according to our definition, and renal acidification defects (RTA) are presented in Table 2. Ten patients who had both hyperuricosuria and RTA had the incomplete form of the defect. Eight had the proximal form and the other 2 the distal form. In the normouricosuric group 7 had the proximal type and 3 the distal type, all of the incomplete form. The duration of the stone disease was the same in both groups. Hyperuricosuric patients had a high operation rate. But when consideration was taken of acidification deflects, only hyperuricosuric patients with RTA exhibited the higher operation rate (Fig. 1). 

Although most of this discussion concerns stones originating in the kidney, lithiasis may be primary to the bladder or the ureters. Whereas phosphate and oxalate stones develop more frequently in the kidney, bladder stones are usually of the urate type. The geographical distribution of urinary lithiasis varies considerably. The disease is common in central Russia, China, Canton, and India. However, in India and China bladder stones are the type seen most often, whereas renal stones are more common in America. 

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