Urolithiasis csbrp
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Urolithiasis csbrp
- 4. Urolithiasis • World wide distribution • 2 % of population • M:F 2:1 • Peak age 2nd to 3rd decade.
- 5. Types 1. Calcium stones 2. Mixed stones ( struvite) 3. Uric acid stones 4. Cystine stones
- 6. Prevalence of various types of Renal stones % of all stones Ca.Oxalate and PhosphateCa.Oxalate and Phosphate 7070 Idiopathic hypercalciuria (50%) Hypercalciuria & hypercalcemia (10%) Hyperoxaluria (5%) Enteric (4.5%) Primary (0.5%) Hyperuricosuria (20%) Hypocitraturia No known metabolic abnormality (15-20%) Magnesium Ammonium Phosphate ((STRUVITE)) 15-20 Uric acidUric acid 5-105-10 Associated with hyperuricemia Associated with hyperuricosuria Idiopathic (50% of uric acid stones) Cystine 1-2 Other or unknownOther or unknown +5+5
- 7. Calcium stones • Most common 75% • Pure stones of Ca oxalate 50% • Pure stones of Ca phosphate 06% • Mixture of Ca oxalate & Ca phosphate 45%
- 8. Etiology of calcium stones • Idiopathic hypercalciuria w/o hypercalcaemia 50% • Hypercalcaemia and hypercalciuria 10% – Hyperparathyroidism – Absorptive hypercalciuria – Renal hypercalciuria • Hyperuricosuria with normal blood uric acid level and without any abnormality of Ca metabolism 15% • Idiopathic Ca stone disease 25% – Unknown, No abnormality in urinary excretion of ca, uric acid and oxalate
- 9. Pathogenesis • Imbalance b/n the degree of supersaturation of ions forming the stone and concentration of inhibition in urine • Nidus – crystals of Ca oxalate, Ca PO4 precipitate in tubular lining around some fragment of debris in tubules • The stone grow, deposition of more crystals at nidus
- 10. Factors contributing stone formation • Urinary alkaline pH • Decreased urinary volume • Increased excretion of oxalate and uric acid
- 11. Morphology • Small less than 1cm • Ovoid, hard SPIKY surface • Dark brown due to blood
- 12. Nephrolithiasis A large stone impacted in the renal pelvis
- 13. Calcium Oxalate Monohydrate Kidney Stone
- 14. Mixed stones (Struvite stones)15 % • Magnesium phosphate • Ammonium phosphate STRUVITE • Calcium phosphate Triple phosphate stones
- 15. Struvite stones
- 16. Struvite stones (Stag horn stone)
- 17. Etiology of Struvite stones • Infection of UT with urea splitting bacteria • Proteus, Klebsiella, Enterobacter • Infection induced stones
- 18. Morphology struvitie stones • Yellow - white or grey • Soft, friable, irregular in shape • Stag horn stone: large solitary stone that takes the shape of renal pelvis
- 20. Uric acid stones. 6%- etiology • Hyperuricaemia, hyperuricosuria • Primary/Secondary gout (due to myeloproliferative dis) • Leukemia on chemotherapy • Administration of uricosuric drugs (Salicylates, Probenicid) • Other factors acid pH less than 6 low urinary volume High nucleic acid turnover
- 21. Pathogenesis of uric acid stones • Solubility of uric acid at pH 7 is 200 mg/dl • at pH 5 is 15 mg/dl • Urine becomes acidic, solubility UA decreases • Prepecipitation of uric acid crystals favours uric acid stones.
- 22. Uric acid stones - 6% • Radiolucent X-ray • But visible on US or CT Radiolucent stones Uric acid Xanthine Triamterene Dihydroxyadenine
- 23. Morphology of uric acid stones • Smooth, yellowish , brown, hard often multiple • Cut surface shows laminated structure
- 24. Cystine stones 2 % etiology Cystinuria Genetically determined Defect in transport of cystine across CM/renal tubules, mucosa
- 25. Pathogenesis of cystine stones • Cystine is least soluble among all aminoacids • Under excess cystineuria- concretion and stone formation
- 26. Morphology of cystine stones • Small round, smooth • Multiple, yellow, waxy
- 27. Other stones less than 2 % • Inherited xanthene metabolism • Xanthinuria • Xanthene stones
- 28. UROLITHIASIS Deficiency of inhibitors of crystal formation •Pyrophosphate •Diphosphonate •Citrate •Glycosaminoglycans •Osteopontin •Nephrocalcin
- 30. Note also that a yellowish- brown calculus formed in the bladder URIC ACID
- 32. HydronephrosisHydronephrosis • Defn: dilatation of renal pelvis and calyces due to partial or intermittent obstruction to the outflow of urine. • Develops due to one or both pelviureteric sphincters incompetence • In the absence of the above there will be dilatation and hypertrophy of urinary bladder, but not hydronephrosis
- 33. Hydronephrosis of the kidney, with marked dilation of the pelvis and calyces and thinning of the renal parenchyma
- 34. Case of hydronephrosis--a ureteral calculus
- 36. Unilateral hydronephrosis Ureteral obstruction at the level of pelviureteric junction 1. Intraluminal- calculi in ureter/renal pelvis 2. Intramural- cong PUJ obstruction – Atresia of ureter – Inflammatory stricture – Trauma – Neoplasms of ureter or bladder 3. Extramural Obstruction of uppr part of ureter by inf renal artery/vein Pressure on ureter from outside ex ca cx, prostate,rectum, caecum, retroperitoneal fibrosis
- 37. Bilateral hydronephrosis • Congenital: Atresia of urethral meatus Cong posterior urethral valve • Acquired: Bladder tumor involving both ureteric orifices Prostatic enlargement Ca prostate, prostatitis Bladder neck stenosis Inflammatory/traumatic urethral stricture & phimosis
- 38. The renal pelvis is markedly dilated, but the ureter is not, indicating that the point of obstruction is the ureteropelvic junction
- 39. Pathologic changes • Depends obstruction, sudden / gradual complete/incomplete Intermittent • Extrarenal / intrarenal
- 40. Extra renal hydronephrosis • Dilatation of renal pelvis medially in the form of sac • As the obstruction persists -Progressive dilation of pelvis/ calyces- pressure atrophy of renal parenchyma • Dilated – pelvicalyceal cystem extends deep in to renal cortex- thin rim of renal cortex streches over calyces- lobulation
- 41. Microscopy –hydronehrosis. • Wall of hydronephrotic sac- fibrous thickening –scarring inflammatory cell infiltrates • Progressive atrophy of tubules, glomeruli • Stasis of urine- infection pyonephrosis.
- 42. E N D
Editor's Notes
- Sometimes a very large calculus nearly fills the calyceal system, with extensions into calyces that give the appearance of a stag's (deer) horns. Hence, the name "staghorn calculus". Seen here is a horn-like stone extending into a dilated calyx, with nearly unrecognizable overlying renal cortex from severe hydronephrosis and pyelonephritis. Nephrectomy may be performed because the kidney is non-functional and serves only as a source for infection. Shown below are typical urinalysis findings for this condition, with evidence for "infection stones" of magnesium ammonium phosphate.
- Triamterene is a potassium-sparing diuretic.
- The passage of a calculus (stone) through the urinary tract is diagrammed here. Calculi form when there is increased excretion of solutes such as calcium and when urine alkalinity, acidity, stasis, and/or concentration are favorable. The most common varieties of calculi are:
- The markedly enlarged prostate seen here has not only large lateral lobes, but a very large median lobe as well that obstructs the prostatic urethra and led to chronic urinary tract obstruction. As a result, the bladder became both enlarged and hypertrophied as it had to work against the obstruction with every episode of urination. That is why the surface of the bladder appears trabeculated. Note also that a yellowish-brown calculus formed in the bladder
- The arrow points to the culprit in this case of hydronephrosis--a ureteral calculus at the ureteropelvic junction. This kidney demonstrates marked hydronephrosis with nearly complete loss of cortex.
- There is scarring of this kidney from chronic obstruction and pyelonephritis. The renal pelvis is markedly dilated, but the ureter is not, indicating that the point of obstruction is the ureteropelvic junction.