Stone disease

Scragg RK, McMichael AJ, Seamark RF. Oral contraceptives, pregnancy, and endogenous oestrogen in gall stone disease—a case-control study. BMJ (Clin Res Ed) 1984 288(6433) 1795-9. 

Pumpkin, Curcubita sp., is a member of the gourd family, Curcubitaceae, that also includes melons, cucumbers, squash, and gac. In 2003, the United States production of pumpkins was approximately 335,000 MT (http //usda.mannlib.comell.edu/ reports/nassr/fruit/pvg-bban/vgan0104.txt). In some mid-eastem African countries, dried pumpkin seeds have been used to treat tapeworm when eaten on an empty stomach (53). Also, for many years in Europe, pumpkin seeds have been used as a remedy for micturition. Pumpkin seed oil has also shown possible beneficial affects in retarding the progression of hypertension (54), potential anti-inflammatory activity in arthritis (55), and may be effective in reducing the risk of bladder-stone disease (56). 

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. 

Tiselius HG. An improved method for the routine biochemical evaluation of patients with recurrent calcium oxalate stone disease. Clin Chim Acta 1982 122(3) 409-18. 

In patients with complex stone disease, adjuvant solution R irrigation can reduce the stone burden, although the overall success rate is limited. However, there is a considerable potential for adverse effects, necessitating close monitoring for sepsis and electroljde abnormalities. 

Joshi HB, Kumar PV, Timoney AG. Citric acid (solution R) irrigation in the treatment of refractory infection (struvite) stone disease is it useful Eur Urol 2001 39(5) 586-90. 

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. 

Taylor EN, Curhan GC. Diet and fluid prescription in stone disease. Kidney Int. 2006 70(70) -835. 

Mandel NS, MandeIGS. Urinary tract stone disease In the United States veteran population. II. Geographical analysis of variations In composition. J.Urol. 1989,142 1516-21. 

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

Following treatment and successful removal of a stone, follow-up monitoring is required, as many patients wiU have recurrent disease in the absence of medical treatment the recurrence rate may be as high as 50% at 10 years. The mechanisms responsible for the multiple recurrences of kidney stones in only certain individuals are not completely understood. Factors involved include (1) urine flow (fluid intake) (2) excretion of excess quantities of stone components (3) the relative absence of a substance, or substances, in the urine that inhibit stone formation and (4) urinary pH (see Figure 45-16). The predominant risk factor is poor hydration, a concentrated urine increasing the concentrations of the mineral salts hirther, predisposing to crystallization. This at least partially explains the increased incidence of kidney stone disease in hot climates, for example, in the Gulf states. 

Ensuring adequate fluid intake remains the cornerstone of management of stone disease. However, specific management of disease depending on the metabolic abnormality present is also unportant and a treatment rationale is emerging. There have been several misconceptions about the role of diet in stone formation and optimal treatment may, at first, appear counter-intuitive some of these paradoxes are discussed below. 

With calcium stone disease, magnesium is an inhibitor of stone growth. Magnesium forms complexes with oxalate that are more soluble than calcium oxalate. Increased urinary magnesium therefore inhibits stone formation. Administration of magnesium has been shown to reduce enteral calcium absorption and has been proposed as a treatment for idiopathic hypercalciuric stone formers. However, oral magnesium supplementation may have unpleasant side effects and a positive benefit in terms of reducing stone recurrence has not been demonstrated. ... 

Some investigators believe that urate may potentiate calcium stone formation, although this perception is not universally accepted. However, hyperuricosuria is common in calcium stone-forming patients, and treatment with allopurinol, thereby decreasing urate synthesis, reduces the rate of stone recurrence. Allopurinol treatment is therefore recommended for hyperuricosuric patients with calcium stone disease. The formation and management of pure urate stones are discussed in Chapter 24. 

Struvite stones (also called triple phosphate or infection stones) are composed of magnesium ammonium phosphate hexahydrate. The formation of such stones requires urinary tract infection with urea splitting organisms and such stones are therefore more common in females and in certain patient populations (e.g, paraplegics), The risk of progression to CKD appears higher in patients who develop infection stones than in other forms of stone disease. 

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. 

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. 

Robertson WG, Peacock M, Heyburn PJ, Marshall DH, Clark PB. Risk factors in calcium stone disease of the urinary tract. Br J Urol 1978 50 449-54. 

Tiselius HG. Metabolic evaluation of patients with stone disease. Urol Int 1997 59 131-41. 

Tiselius HG. Possibilities for preventing recurrent calcium stone formation principles for the metabolic evaluation of patients with calcium stone disease. 

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. 

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). 

Dretler SP. The physiologic approach to the medical management of stone disease. Urol CUn North Am 1998 25 613-623. 

Endemic bladder stone disease still occurs in the western population, but a clear relationship exists between a decreasing incidence of bladder stone development and growing prosperity (Bl). An increase in the incidence of upper urinary tract stone formation has been seen during recent decades. The diet of an affluent lifestyle induces metabolic changes that increase the risk of calcium-containing stones forming in the urinary tract. Because protein-rich food is more readily available to affluent persons, their urinary excretion of calcium, oxalate, and urate is increased whereas urinary pH and excretion of citrate are reduced (Bl). The... 

The reoccurrence of urolith formation following a primary episode is referred to as recurrent stone disease, irrespective of the stone s composition or localization, or the time interval following the first stone episode. This term does not include continuous crystalluria without clinically manifest concrements (S3). 

Dent s disease and other kidney stone diseases Osteopetrosis Bartter s syndrome Kidney disease Glomerulosclerosis, defective Mg reabsorption Mucolipidosis IV Malignant hyperthermia, central core... 

Cal Kulis is an 18-year-old boy who was brought to the hospital by his mother because of the sudden onset of severe pain in the left flank radiating around his left side toward his pubic area. His urine was reddish-brown in color, and his urinalysis showed the presence of many red blood cells. When his urine was acidified with acetic acid, clusters of flat hexagonal transparent crystals of cystine were noted. An x-ray of his abdomen showed radiopaque calculi (stones) in both kidneys. There was no family history of kidney stone disease. 

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. 

Wesson, J. A. and Ward, M. D. 2006. Role of crystal surface adhesion in kidney stone disease, Curr... 

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

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