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Renal calculi

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NUMAN SHAH IPMS-KMU/HMC
NUMAN SHAH IPMS-KMU/HMC

This document summarizes renal calculi (kidney stones). It defines renal calculi and lists its common types, including calcium oxalate, phosphate, uric acid, and cystine stones. The pathogenesis of different stone types is discussed, such as hypercalciuria leading to calcium oxalate stones and urinary tract infections causing struvite stones. Common sites of stone formation are the renal pelvis, calyces, and urinary bladder. Predisposing factors include metabolic abnormalities, dehydration, urinary stasis, and renal diseases. Complications include pyelonephritis, urinary retention, and renal failure. Clinical features range from gross hematuria and flank pain to symptoms of acute obstruction

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Renal Calculi Numan Shah 2nd Batch Renal Dialysis
Outlines Defination of renal Calculi & its types Pathogensis Common sites Predisposing factors Copmlications Clinical features
Renal Stones Urolithiasis Renal Calculi Nephrolithiasis Kidney Stones
Urolithiasis(renal stones) Definition: The stone formation within the kidney or collecting system is called Urolithiasis OR Urolithiasisis calculus formation at any level in the urinary collecting system kidney (nephrolithiasis), ureter (ureterolithiasis), bladder (cystolithiasis),
Types of renal stones Common stones: OXALATE (CALCIUM OXALATE) PHOSPHATE URIC ACID / URATE CYSTINE
Un-common XANTHINE STONES (Autosomal Recessive . Def of Xanthine Oxidase leading to Xanthinuria) DIHYDROXY ADENINE STONE ( Def. of enzyme adenine phospo ribosyl transferase ) SlLICATE STONES Rare in humans ( excess intake of Antacid with Mg Trisilicate. Mostly in cattle due to ingestion of Sand ) MATRIX - Infection by Proteus - Radiolucent (all calculi have some amt ( 3%) of matrix but matrix calculus has 65% Matrix content in calculi)
Types of stones Calcium oxalate stones: Most common type (70%) containing calcium oxalate or calcium oxalate mixed with calcium phosphate Triple phosphate stones: (15%) composed of magnesium ammonium phosphate Urate stones: About (10%) copmmposed of uric acid Cystine stones: (1-2%) made up cystine
Pathogenesis Calcium oxalate stones Hypercalcemia: About (10%) of patients have hypercalcemia due to hyperparattyroidism, or vitamin D intoxication etc. Hypercalciuria: About (55%) have hypercalciuria without hypercalcemia (idipathic hypercalciuria). Probably it results from hyperabsorption from calcium from intestine or impairment in renal tubular reabsorption of calcium Idiopathic: In about 20% patients,stone formation occurs without either hypercalcemia or hypercalciuria
Pathogenesis Triple phosphate stones: The magnesium ammonium phosphate (struvite) stones usually follow the infection by urea splitting bacteria(proteus and stayphlococcus) which convert urea to ammonia,producing urine alkaline in which magnesium ammonium phosphate salts precipitate to form stone.
Patogenesis Urate stones: Composed by Uric acid Caused by high intake of protein diet and gout Cystine stones: They are associated with genetically determined defect in the renal transport of cystine aminoacid.
Common sites of stone formation Renal pelvis Calyces Urinary bladder
Predisposing factors Metabolic factors: Hypercalciuria Hyperphosphaturia Oxaluria Uric acid excess Dehydration: Causing increased urinary concentration
Predisposing factors Stasis: Obstruction to urine flow encourages salt precipitation Urinary pH:Uric acid and oxalate stones form in an acidic urine,while the phophate stones develop in an alkaline urine Renal disease: Renal infections(producing urine alkaline) Renal Tumors (producing renal stasis)
Copmlications Pyelonephritis Acute urinary retension Recurrent chances of infection Renal failure Pyonephrosis
Clinical features Gross hematuria Nausea and vomiting Frequent or painful urination Dull pain when stone remains in kidney Episode of flank pain radiating to the groin when small stones pass into the ureters
Clinical features Acute obstruction of ureter--- severe colic Flank pain referred to genitalia Nausea, vomiting Microhematuria Chronic stone distends to be associated with large or multiple stones can be little or no pain may have impaired renal function, anemia, weight loss etc. concomitant infection more likely
Renal calculi
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Renal calculi

  • 1. Renal Calculi Numan Shah 2nd Batch Renal Dialysis
  • 2. Outlines Defination of renal Calculi & its types Pathogensis Common sites Predisposing factors Copmlications Clinical features
  • 4. Urolithiasis(renal stones) Definition: The stone formation within the kidney or collecting system is called Urolithiasis OR Urolithiasisis calculus formation at any level in the urinary collecting system kidney (nephrolithiasis), ureter (ureterolithiasis), bladder (cystolithiasis),
  • 5. Types of renal stones Common stones: OXALATE (CALCIUM OXALATE) PHOSPHATE URIC ACID / URATE CYSTINE
  • 6. Un-common XANTHINE STONES (Autosomal Recessive . Def of Xanthine Oxidase leading to Xanthinuria) DIHYDROXY ADENINE STONE ( Def. of enzyme adenine phospo ribosyl transferase ) SlLICATE STONES Rare in humans ( excess intake of Antacid with Mg Trisilicate. Mostly in cattle due to ingestion of Sand ) MATRIX - Infection by Proteus - Radiolucent (all calculi have some amt ( 3%) of matrix but matrix calculus has 65% Matrix content in calculi)
  • 7. Types of stones Calcium oxalate stones: Most common type (70%) containing calcium oxalate or calcium oxalate mixed with calcium phosphate Triple phosphate stones: (15%) composed of magnesium ammonium phosphate Urate stones: About (10%) copmmposed of uric acid Cystine stones: (1-2%) made up cystine
  • 8. Pathogenesis Calcium oxalate stones Hypercalcemia: About (10%) of patients have hypercalcemia due to hyperparattyroidism, or vitamin D intoxication etc. Hypercalciuria: About (55%) have hypercalciuria without hypercalcemia (idipathic hypercalciuria). Probably it results from hyperabsorption from calcium from intestine or impairment in renal tubular reabsorption of calcium Idiopathic: In about 20% patients,stone formation occurs without either hypercalcemia or hypercalciuria
  • 9. Pathogenesis Triple phosphate stones: The magnesium ammonium phosphate (struvite) stones usually follow the infection by urea splitting bacteria(proteus and stayphlococcus) which convert urea to ammonia,producing urine alkaline in which magnesium ammonium phosphate salts precipitate to form stone.
  • 10. Patogenesis Urate stones: Composed by Uric acid Caused by high intake of protein diet and gout Cystine stones: They are associated with genetically determined defect in the renal transport of cystine aminoacid.
  • 11. Common sites of stone formation Renal pelvis Calyces Urinary bladder
  • 12. Predisposing factors Metabolic factors: Hypercalciuria Hyperphosphaturia Oxaluria Uric acid excess Dehydration: Causing increased urinary concentration
  • 13. Predisposing factors Stasis: Obstruction to urine flow encourages salt precipitation Urinary pH:Uric acid and oxalate stones form in an acidic urine,while the phophate stones develop in an alkaline urine Renal disease: Renal infections(producing urine alkaline) Renal Tumors (producing renal stasis)
  • 14. Copmlications Pyelonephritis Acute urinary retension Recurrent chances of infection Renal failure Pyonephrosis
  • 15. Clinical features Gross hematuria Nausea and vomiting Frequent or painful urination Dull pain when stone remains in kidney Episode of flank pain radiating to the groin when small stones pass into the ureters
  • 16. Clinical features Acute obstruction of ureter--- severe colic Flank pain referred to genitalia Nausea, vomiting Microhematuria Chronic stone distends to be associated with large or multiple stones can be little or no pain may have impaired renal function, anemia, weight loss etc. concomitant infection more likely