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Obstructive Uropathy

Obstructive Uropathy. Dr Rodney Itaki Lecturer Anatomical Pathology Discipline. University of Papua New Guinea School of Medicine & Health Sciences Division of Pathology. Some Definitions. Hydronephrosis- Dilation of the renal pelvis or calyces

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Obstructive Uropathy

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  1. Obstructive Uropathy Dr Rodney Itaki Lecturer Anatomical Pathology Discipline University of Papua New Guinea School of Medicine & Health Sciences Division of Pathology

  2. Some Definitions • Hydronephrosis- Dilation of the renal pelvis or calyces • Obstructive uropathy- functional or anatomic obstruction of urine flow at any level of the urinary tract • Obstructive nephropathy- when obstruction causes function or anatomic renal damage

  3. Anatomy Review

  4. Types of Obstruction Ref: Robins Pathological Basis of Diseases, 6th Ed.

  5. Causes of Obstruction

  6. Prevalence • 3.1% in autopsy series • No gender differences until 20 years • Females more common 20-60 • Males more common older than 60 • 2-2.5% of children at autopsy • PNG Population unknown Ref: Jamie Bartley Teaching Slides, Detroit, 2009

  7. Pathophysiology • Effects variable and depend on whether the obstruction is unilateral or bilateral. • Mechanical obstruction of urine outflow results in: • Increase backflow pressure into kidneys • Stagnation of urine • Increased risk of infection • Increased risk of formation of stones • Induce non-infective inflammation in interstitial tissue of kidneys • Progressive dilation of renal pelvis and calyces • Progressive atrophy of renal parenchyma Ref: Robins Pathological Basis of Diseases, 6th Ed.

  8. Morphology Dilation of perlvis & calyces depends on whether obstruction is sudden & complete or incomplete and chronic • Sudden & complete – reduced GFR leads to mild dilation and atrophy of renal parenchyma • Subtotal or intermittent - normal GFR leads to progressive dilation Ref: Anjali Shinde Teaching Slides

  9. Hydronephrosis Ref: Robins Pathological Basis of Diseases, 8th Ed.

  10. Morphology • Chronic cases – cortical atrophy and diffuse institial fibrosis. • Advanced stages – kidneys become a thin wall cystic structure, significant parenchymal atrophy and obliteration of renal pyramids and thin cortex.

  11. Clinical Presentation • Acute obstruction – pain (renal colic) if calculi lodged in ureters. Prostatic enlargement cause urinary symptoms. • Unilateral complete or partial hydronephrosis - asymptomatic for long periods of time. Present late. • Bilateral partial obstruction – polyuria and nocturia (unable to concentrate urine). • Hypertension common in chronic cases • Acute complete bilateral obstruction – oliguria, anuria and azotemia. Surgical Emergency.

  12. Prognosis • Depends on site, partial or complete, acute or chronic and duration of obstruction. • Generally if diagnosed early and obstruction relieved, recovery is good with return to normal kidney function. • Late diagnosis – chronic renal failure.

  13. Urolithiasis (Renal Calculi, Stones) • 4 types of stones • Calcium oxalate (phosphate) – 75% • Struvite (Magnesium Ammonium Phosphate) – 10-15% • Uric Acid – 6% • Cystine – 1-2% • Unknown - ?10%

  14. Pathogenesis • Calcium oxalate stones – hypercalcemia and hypercalciuria from various causes • Magnesium ammonium phosphate stones – infections from urea splitting bacteria (e.g. Proteus and some staphylococci). • Uric acid stones – hyperuricemia (e.g. gout, leukemias). However, >50% of patients with urate stones do not have hypeuricemia nor increased urine uric acid excretion • Cystine stones – caused by genetic defects in renal reabsorption of amino acids & cystine.

  15. Urolithiasis Pathogenesis • Cystine stones form at low urinary Ph. • Risk factors for kidney stone formation: • increased concentration of stone constituents (saturated and thus precipitate) • Changes in urinary Ph (low Ph, higher risk). • Decreased urine volume • Urinary tract infection • However, many calculi occur in the absence of these factors. ? Deficiency of inhibitors of crystal formation. Long list. Read up.

  16. Site of Kidney Stone Formation • Unilateral in 80% • Renal calyces and pelves common sites • small (2-3 mm) • smooth or irregular spiked edges • Bladder • Staghorn calculi - large stone at pelvis forming a cast of the pelvic and calyceal system.

  17. Clinical Presentation of Kidney Stones • Symptoms appear if causing obstruction, or produce ulceration and cause bleeding. • Can by asymptometic • Smaller stones pass into ureters producing intense pain (renal colic). • Hematuria • Recurrent UTI

  18. Laboratory Diagnosis • UEC • BUN • Urinalysis – hematuria, crystals, pyuria • Other modes of investigation – USS, X-ray, CT

  19. Prognosis – Kidney Stone • Generally good. • Depends on underlying cause of kidney stone formation

  20. End Main Reference: Robins Pathological Basis of Diseases, 6th Ed. Chapter on The Pancreas. Download seminar notes on: www.pathologyatsmhs.wordpress.com File in PDF and PPT format

  21. Feedback What was presented well and you understood concepts? What was not presented well and not understood well? How can seminar be improved? Go to www.pathologyatsmhs.wordpress.comand leave feedback comments

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