Most common kidney stones are of calcium oxalate1, 10 to 12% of them contain uric acid2, while most have small amount of hydroxyappetite. Stones containing struvite, pure uric acid, combination of hydroxyappetite and calcium monohydroxy phosphate and a few containing cystine are also found. Calcium oxalate and calcium phosphate stones are black, grey or white, smaller than 1 cm in diameter, dense opaque and sharply circumscribed. Uric acid stones are white or orange and crystals are radio graphically transparent. Simple urinalysis can reveal the presence of crystals and provide clues to the stone type. To analyse the composition and differentiation of renal stones, polarization microscopy3, infrared and X-ray diffraction4 techniques are modern methods. CT scan is used to differentiate transparent stones from renal tissue or blood clots5. Renal stone formation depends upon the concentration of different salts in urine. In normal urine concentration of calcium oxalate salts is four times higher than its solubility, increased excretion of calcium and oxalate with less urinary volume increases calcium oxalate supersaturation and when it is 7-11 times the normal solubility, enucleation of calcium oxalate starts and possible surfaces for it in kidney are epithelial lining, cell debris, urinary cast and other crystals6. Any factor increasing heterogenous nuclei in tubular fluid or urine like epithelial injury lowers the upper metastable limit (super-saturation at which crystals first form), hyperuricosuria lowers the metastable limit by promoting calcium oxalate stone formation7,8. Hypercalciurea and hyperuricurea promote haematuria probably from crystal urea. Calcium phosphate super saturation occurs at urinary pH of 6.5 due to high proportion of divalent and trivalent phosphate ions. Microscopic nuclei can form stones by growing or aggregating into large clumps, but they cannot grow enough to anchor and occlude renal tubular lumen within 5 to 7 seconds, as they pass through nephron very rapidly but they can do so in one minute9. Kidney proteins inhibit all phases of crystalization. Nephrocalcin containing r-carboxyglutarnic acid, inhibit calcium oxalate stone formation10-13. Famm-Horsfall mucoprotein from renal thick ascending limb, inhibit aggregation of calciumoxalate crystals14. Uropontin by kidney inhibits the growth of calcium oxalate crystals. Patients with renal lithiasis present with intense pain radiating from flanks to anterior side of thigh -associated with nausea, vomiting15, urinary frequency and dysuria as stone passes towards ureterovesical function. If it passes into bladder, decompression of urinary tract relieves pain spontaneously. Stone may cause obstructive uropathy if painless and remains undetected for a long time. Management of stones depends upon its site, size and type. Most ureteral stones less than 5mm in diameter pass readily, but 7 mm in diameter or larger stones have a poor chance of passing. Stones lodged in distal ureter, not progressing are best removed uretroscopically with a stone basket or disrupted in situ with extra corporeal shockwave lithotripsy (ESWL) 16-18. Stones embedded in proximal ureter are pushed upwards in renal pelvis and disrupted by ESWL, it requires a cystoscopy to push the stone backwards by a catheter up the ureter. If double J stent is passed up the renal pelvis, it improves the chances of complete stone removal18. Percutane Our nephrolithotomy is needed if lithotripsy fails. Surgical ureterolithotomy should only be used as a last resort. Kidney stones that are less than 2 cm but more than 5 mm in diameter can best be treated with ESWL. Stones exceeding 2 cm or of 1 mm diameter lying in lower renal pole should be treated with percutaneous nephrolithotomy17-19. because of the use of lithotripsy alone leaves residual stones in 35 to 54% cases, whereas percutaneous nephrolithotomy succeeds in most17-19. Double J stent facilitates the complete drainage of fragments specially in case of large stones. Asymptomatic kidney stones of less than 5 mm should be left untreated. Etiological bases of stones is another important aspect for its treatment and prevention of recurrence. People with primary hyperparathyroidism excrete a high fraction of dietary calcium and in these cases 1 a 25 dihydroxy colcalciferol, increases the intestinal absorption of calcium20, raises renal tubular calcium resorption21 and bone turnover leading to hypercalcaemia, hypercalciurea22,23 and lowering of phosphorus resorption. Low serum phosphorus levels enhance the calciferol production, which in turn causes hypercalciurea24,25. In people with familial idiopathic hypercalciurea, erythrocyte calcium ATPase levels may vary directly with the level of urinary calcium excretion26. People having hypercalciurea as a result of high serum calcitriol levels caused by renal phosphate wasting is reversed by oral phosphate supplements. Pseudoxanthoma elasticum causes high levels of calcitriol and hypercalciurea27, cystic fibrosis causes hypercalciurea and nephrocalcinosis28. Consanguineous marriages in hypercalciuric families raise the chances of hypercalciurea in successive generation with Increased rate of calcium excretion. Pak and colleagues28 have proposed two types of idiopathic hypercalciurea. All patients with absorptive hypercalciurea have normal or low levels of serum parathyroid hormone and fasting urinarylevels below. 11 mg per dl. of creatinine clearance28. Thiazide diuretics lower urinary calcium excretion by increasing fractional calcium resorption through distal nephron and reducing intestinal absorption29,30. Renal tubular acidosis in patients with idiopathic hypercalciurea is due to papillary calcification, so mainly calcium phosphate stones are formed31 and these people respond to thiazide diuretics whereas potassium alkali ratio are useful in patients with hypercalciurea due to metabolic acidosis32. Calcium oxalate stones are not very common but they can invade the urinary tract, cause pain, bleeding and then disperse, passed as gravel also called ‘crystalurea’. A simple dietary excess of oxalate from food like spinach, rhubarb, coco, beet, peanut, pepper, wheat germ and chocolates cause hyperoxalurea33,34 (20-40 mg per day is normal). Malabsorption from small bowel from any cause including resection intrinsic disease, jejunal bypass, etc., expose the mucosa to detergents like bile salts and fatty acids which increase its permeability to oxalates35,36. Treatment includes reducing the dietary oxalate and fats37, oral calcium supplements as carbonate salts and oral citrate supplements thatprecipitate oxalate in intestinal lumen. High fluid intake is also advised. Patients with hyperoxalurea respond to pyridoxin supplements and increased urinary volume to 3 litres. Uric acid stones are found in pure as well as combined with others. These are treated by raising the pH to 6-6.5 with potassium alkali salts. Allupurinol is beneficial in cases of 1200 mguric acid excretion per day. Urinary infection with bacteria that express urease cause struvite (magnesium ammonium phosphate) stone38. These are associated with bleeding obstruction or infection. They require removal; ESWL39 or percutaneous nephrolithotomy to reduce their growth. Once patient is free of stone, antibiotics are beneficial. Increasing urinary pH and volume to 4 litre per day prevents cystine stones which is associated with cystineurea and dehydration. Penicillamine or tiopronin combined with cystine to form a soluble salt and reduce the stone formation. So they are also useful for its treatment40.
1. clinical approach. in nephrolithhiasis: pathogenesis and treatment by F.L coe and J.H. Parka. 2nded. chicago, Year Book 1988, pp. 1-37.
2. MIllman, S., Strauas, AL., Parks. J.H. and Coe, FL Pathogenesis and clinical courae of mixed calcium oxalate and uric add nephrolithiasis. Kidney tnt., 1982; 22:366-70.
3. Herring, LC. Observations on the analysia of ten thousand urinary calculi. J.Urol., 1962;88:545-62.
4. Otnes, B. Urinary stone analysis method, materials and value. Scandi.Urol.Nephrol. (SuppL), 1983;71:1-109.
5. Brand, E., Harris. M.M. and Biloon, S. Cystin urea, the excretion of a cyatin complex which decomposes in the urine with the libration of free cyatin. J.Biol. Chem., 1930;86:315-31.
6. Brown, C.M. and Purich, D.L Physical-chemical processes in kidney stone formation in disorders of bone and mineral metabolism. Edited by EL Coe and Mi Paws. New York. Raven Press, 1992, pp.613-24.
7. Uric add and calcium oxalate atones in nephrolithiaaia: psthogeneaia and treatmentby F.L Coeand J.H. Parks. 2nded. chicago, Year Book, 1988; pp. 205-31.
8. Pat, CY.C, Barilla, D.E., Holt, K., Brinkley, L., Tolentino, It and Zerwekh,3.E Effect of oral purine load and allopurinol in the csystslization of calcin salts inurine of patients with hyperuricosuric calcium urolithiasis. Am.J.Med., 1978;65:593-99.
9. Kok, I.T., Papapolous. S.E. and Brijvoet, O.LM. Crystal agglomeration ia a major element in calcium oxslate urinary atone formation. Kidney Int., 1990;37:51-56.
10. Nakagsws, Y., Abram, V., Parka, J.H., Lsu, H.S.H., Kswooys, 1K. and Coe, EL Urine glycoprotein crystal growth inhibitor evidence for a molecular abnormality In calcium oxalate nephrolithissia. J.Clin.Invest., 1985;76:1455-62.
11. Nakagawa, Y., Ahmed, M., Hall, S.L., DeGsnello,S. and coe, EL Isolation from human calcium oxalate renal stones of nephrocslcin, a glycoprotein inhibitor of calcium oxalate crystal growth. Evidence that nephrocalcin from patients with calcium oxslate nephrolithissis is deficient in gamma-carboxyglutamic acid J.Clin.Invest., 1987;79.1782-87.
12. Worcester, EM., Nsksgawa, Y., Webner, CL, Kumsr, 5. and Coe, P.L Crystal absorption and growth slowing by nephrocaldum, albumin and Fsmmhorafall protein. Am.J.Phyaiol.. 1988;255:F1197- F1205.
13. Arplin, 3., DeGanello, S., Nakagswa, Y.N. and coe, ELEvidence thatnephrocalcinand urine inhibit nucleation of calcium onlate monohydrste crystals. Am.J.Physiol., 1991;261:F824-3ft
14. Hess, B., Nsksgsws, Y., Parks, J.H. and Coe, F.L Molecular sbnormslity of Pamm-Horsfall glycoprotein in calcium oxslste nephrolithiasis. Ami.PhysioL, 1991;260:F569-78.
15. Bretlsnd, P.M. Acute uretericobatruction. London, Butterworths, 1972, pp. 1-219.
16. Blute, ML, Segura, J.W. and Pstteraon, D.E. Ureteroscopy. J.Urol., 1988;139:510-12.
17. Seguara, J.W. The role of percutaneous surgery in renal and ureteral atone removsL .J.Urol., 1989;141:780-81.
18. Lingeman, I.E. Mechanism of stone disruption and dissociation, in disorderaof bone and mineral metabolism. Edited by F.L Coe and Mi. Fsvus. New York, Raven Press, 1992, pp. 625-70.
19. Lingemsn, I.E., Woods, J., Toth, P.D., Evan, A.P. and McAteer, J.A. The role of lithotripay and its side effects. J.Urol., 1989;141:793-97.
20. Fsvus, Mi. Intestinal absorption of calcium, msgneaium and phosphorus in disorders of bone and mineral metabolism. Edited by P.L Coe, M.J. Paws. New York, Raven Press, 1992, pp. 57-82
21. Ysnagaws, N. and Lee, D.B.N. Renal handling of calcin and phosphorus, in disordera of bone and mineral metabolism. Edited by P.L coe, Mi. Favus. New York, Raven Press, 1992, pp. 3-40.
22. Coe, F.L and Bsshinski, D.A. Pathophysiology of hypercalciurea. Ami.Physiol., 1984:247(1 Pt.2):F1-F13.
23. Parks, J., Coe, F.L and Paws, M. Hyperpsrsthyroidism in nephrolithissis. Arch.Intern.Med., 1980;140:1479-81.
24. Consensus Development Conference Panel Diagnosia and management -of ssymptomatic primary hyperpsrathyroidism. Consensus Development Conferences Statement Ann.Intern.Med., 1991;114:593- 97.
25. Halabe. A and Sutton, R.A.L Primary hyperpsrathyroidism as a cause of calcium nephrolithissis in disordera of bone snd mineral metabolism. Edited by F.L Coe and M.J. Paws. New York, Raven Prms, 1992, pp.671-84.
26. Bisnchi, G., Vezzoli, G., Cusi, D.. Cova, T.. Elli, A., Soldati, L, Tripodi, G. et sL Abnormal red cell calcin pump in patients with idiopathic hypercalciures. N. EngI. J. Med., 1988;319:897- 901.
27. Manette, LE. and Hechanick, J.L Heritable syndrome of prudozenthoms elssticum with abnormal phosphorus sndvitamin D metabolism. Ami.Med., 1987;83:1157-61
28. Pak, CY., Britton, F., Peteraon, It, Ward, D., Northcutt, C, Breslau, NA, McGuire, J., Sskhaee, K., Bush, S., Nicar, M., Norman, D.A. and Peters, P. Ambulatory evaluation of nephrolithiasis. Classification, clinical presentation and diagnostic criteria. Am. 3. Med., 1980;69:19-30.
29. Coe, F.L, Parks, J.H., Buahinsky, D.A., Lsngmsn, CB. and Paws, Mi. Clorethalidone promotes mineral retention in patients with ideopsthic hypercalciures. Kidney tnt., 1988;33:1140-46.
30. Shimizu, T., Nsksmura, M., Yoshitomi, K. and l~ai~ M. Interaction of trichior metriazide or aniloride with PTH in stimulating Ca + absorption in rabbit CNT. Am.J.Physiol., 1991;261:F36.F43.
31. Carnans, R.J. and Buckalew, V.M. Jr. The syndrome of distill (type 1) renal tubular scidosis: dinicaland laboratorytindingin58cases. Medicine (Baltimore), 1988;67:84-99.
32. Coe, F.L and Parks, J.H. Stonedisesse in hereditary distill renal tubular acidosis. Mn. Intern. Med., 1980;93:60-61.
33. Hayasbi, Y., Kaplan, LA. snd Psrks,CY. Effect ofsodium cellulose phosphatetherspy on crystalizstion of calcium oxalate in urine. Metabolism, 1975;24:1273-7&
34. Jseger, P., Portmsnn, L, lacquer, A.E and Burckhardt, P. Influence of the calcium content of the diet on the incidence of mild hyperoxsluria in ideopsthic renal stone formers. Am.J.Nephrol., 1985;5:40-44.
35. Dobbins, J.W. and Binder, Hi. Effect of bile salts and fstty scids on the colonic absorption of oxalate Gastroenterology, 1976;70:1096-1100.
36. Csthpulir, S.C, Paws, Mi. and Coe, P.L Evidence forsize and charge permselectivity of rat sscending colon; effects of ricinoleste and bile salts on oxalic acids and neutral sugar transport.J.Clin.Invest., 1984;74:805-11.
37. Smith, LH. Hyperoxsluric states in disorders of bone and mineral metabolism. Edited by FL Coe and M.J. Paws. New York, Raven Press, 1992, pp,707-82.
38. Coe, EL and Parks, J.H. Nephrolithiasis: psthogenesis and treatment 2nd ed. Chicago, Year Book, 1988.
39. Krinstensen, C., Parka, J.H., Undherimer, M. and Coe, EL Reduced glomerular filtration rate and hypercslciures in primsry struvite nephrolithissis. Kidney int., 1987;32:749-53.
40. Geeron, Mi., Kobashi, K. snd Griffith, D.P. Non-calcium nephrolithissis in disorders of bone and mineral metabolism. Edited by EL Coe and Mi. Fsvus. New York, Raven Press, 1992, pp. 801-29.