Chapter 32: Alterations of Renal and Urinary Tract Function

Urinary tract obstruction impairs urine flow through structural or functional abnormalities, causing hydronephrosis and progressive nephron damage. Upper urinary tract blockages from nephroliths form through mineral supersaturation and crystallization, with composition including calcium oxalate, struvite, uric acid, and cystine variants. Risk factors, stone formation mechanisms, clinical presentation with flank pain and hematuria, and therapeutic interventions from conservative management to extracorporeal shock wave lithotripsy and surgical removal are integrated with understanding of how obstruction reduces glomerular filtration and initiates tubulointerstitial fibrosis. Lower tract obstructions and neurogenic bladder dysfunction, including detrusor overactivity and sphincter dyssynergia, arise from neurologic injury or outlet resistance abnormalities. Renal cell carcinoma and urothelial tumors present insidiously with hematuria and require multimodal imaging and surgical intervention. Urinary tract infections spanning acute bacterial cystitis, chronic pyelonephritis, and painful bladder syndrome involve uroepithelial invasion, inflammatory cascades, and antimicrobial resistance patterns. Glomerular disease pathophysiology centers on immune-mediated injury through circulating immune complex deposition or anti-glomerular basement membrane antibody formation, producing nephrotic and nephritic syndrome patterns with characteristic urinary findings, proteinuria, and progressive sclerosis. Acute kidney injury develops through prerenal hypoperfusion, intrarenal acute tubular necrosis from ischemic or toxic insult, or postrenal obstruction, with severity stratified using standardized classification systems. Chronic kidney disease represents irreversible nephron loss and declining glomerular filtration rate, most commonly from diabetes mellitus or hypertension, triggering multisystem complications including renal osteodystrophy, cardiovascular remodeling, anemia, uremic encephalopathy, and immunologic dysfunction. Management strategies address underlying disease, prevent progression, manage mineral-bone disease, control hypertension, and employ renal replacement therapies including dialysis and transplantation.