RENAL DISEASE - Auburn University

RENAL DISEASE - Auburn University

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: Structure predisposes it to immune complex deposition and complement fixation Tubules: Post-Renal Structures (ureters, bladder) Malformations, Obstruction, Masses (i.e. cancer) 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.

Glomerular Capillary: Normal versus Pathology 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. Goodpastures Syndrome: Antibody binding to GBM 6. Glomerular injury with proteinuria: Podocyte effacement

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

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 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

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?

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 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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