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RENAL DISEASE: OVERVIEW AND ACUTE RENAL FAILURE Pathophysiology of Disease: Chapter 16 (388-394)

RENAL DISEASE: OVERVIEW AND ACUTE RENAL FAILURE Pathophysiology of Disease: Chapter 16 (388-394). Jack DeRuiter, PhD Department of Pharmacal Sciences April, 2000. Kidney Sites Susceptible to Renal Disease (page 388). General: Renal medulla: Low oxygen environment: Ischemia Glomerulus:

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RENAL DISEASE: OVERVIEW AND ACUTE RENAL FAILURE Pathophysiology of Disease: Chapter 16 (388-394)

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  1. RENAL DISEASE:OVERVIEW AND ACUTE RENAL FAILUREPathophysiology of Disease: Chapter 16 (388-394) Jack DeRuiter, PhD Department of Pharmacal Sciences April, 2000

  2. Kidney Sites Susceptible to Renal Disease (page 388) • General: Renal medulla: • Low oxygen environment: Ischemia • Glomerulus: • Structure predisposes it to immune complex deposition and complement fixation • Tubules: • “Post-Renal” Structures (ureters, bladder) • Malformations, Obstruction, Masses (i.e. cancer)

  3. CATEGORIZATION • Generalized Site of Disease: • Prerenal: Inadequate renal blood flow • Intrarenal: Nephron damae • Postrenal: Obstruction, Structural defects • Site of Renal Lesion (Intrarenal) • Glomerulopathy • Nephritic: • Nephrotic: • Tubulointerstitial Disease • Etiologic Factors: Infection, Diabetes, etc.

  4. Glomerular Capillary: Normal versus Pathology

  5. Glomerular Capillary Pathology(see previous slide) 1. Membranous nephropathy: Subepithelial deposits 2. Post-infectious glomerulonephritis: Subepithelial 3. Lupus glomerulonephritis: Subendothelial deposits 4. IgA Nephropathy: Mesangial deposits 5. Goodpasture’s Syndrome: Antibody binding to GBM 6. Glomerular injury with proteinuria: Podocyte effacement

  6. Nephrotic vs Nephritic Disorders • Nephrotic: • profound proteinuria • Immune complex deposits: Epithelial • NO cellular inflammatory reaction • Nephritic: • Variable proteinuria • Immune complex deposits: Subendothelial or GBM • Cellular inflammatory reaction

  7. ACUTE RENAL FAILURE:Clinical Presentation (pages 389-390) • Heterogeneous group of disorders characterized by rapid deterioration in renal function (Decreased GFR) • Rapid elevation of BUN and serum creatinine • Oliguria: Variable • Other: Henaturia, proteinuria, edema, hypertension

  8. ACUTE RENAL FAILURE:Etiology (page 390 and Table 16-3) • Prerenal: • CV and volume depletion • Drug-induced or related (NSAIDs, ACEIs, diuretics) • Intrarenal: • Inflammatory disease: Vasculitis, glomerulo-nephritis, drug-induced • Acute tubular necrosis • Postrenal: Obstruction, Cancer, congenital abnormalities

  9. ACUTE RENAL FAILURE:Pathology (pages 390-392) • Acute tubular necrosis (ATN): • Tubular cell sloughing • Reversibility/Irreversibility: Dependent on time of intervention • ATN Pathogenesis • Tubular occlusion theory and cast formation • Vascular hypoperfusion theory: Afferent vasoconstriction with Efferent vasodilation • Role of renal mediators?

  10. ACUTE RENAL FAILURE:Early Clinical Manifestations (pages 392-394) • Symptoms depend on degree and cause of renal failure (See Table 16-5) • Initial Symptoms: Fatigue and malaise: • Loss of excretory capacity and accumulation of water, electrolytes and nitrogenous wastes • Prerenal azotemia: Elevated BUN/SrCr (20-30:1) with normal SrCr • Urinalysis: No casts detected • Maximal urinary concentration: 1500 mosm/L • Fractional Na Excretion (99%) • May progress to ATN without proper treatment

  11. ACUTE RENAL FAILURE:Later Clinical Manifestations (pages 392-394) • Later Symptoms (frank ATN): dyspnea, orthopnea, heart (sound S3), edema • Normal BUN/SrCr, profressive elevation of SrCr • Casts (protein, RBC, epithelial cells) • Urine osmolality • Fractional excretion of Na (as low as 1%)

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