1- Urinary obstruction and stasis

Urinary Obstruction and Stasis

• Urinary tract obstruction can occur during fetal development, childhood, or adulthood.
• Obstruction location can be proximal (calyces) or distal (urethral meatus).
• Renal obstruction leads to permanent damage, limiting metabolic waste excretion, and altering water and electrolyte balance.

Renal

• Congenital: Polycystic kidney, renal cyst, peripelvic cyst, ureteropelvic junction obstruction, Wilms tumor
• Neoplastic: Renal cell carcinoma, transitional cell carcinoma of the collecting system, multiple myeloma
• Inflammatory: Tuberculosis, Echinococcus infection
• Metabolic: Calculi, sloughed papillae
• Miscellaneous: Trauma, renal artery aneurysm

Bladder and Urethra

• Congenital: Posterior urethral valve, phimosis, hydrocolpos
• Neoplastic: Bladder carcinoma, prostate carcinoma, carcinoma of urethra, carcinoma of penis, paraurethral abscess, neurogenic bladder
• Inflammatory: Prostatitis
• Miscellaneous: Benign prostatic hypertrophy

Definitions

• Hydronephrosis: Dilation of the renal pelvis or calyces, often associated with obstruction, but can be present without it.
• Obstructive uropathy: Functional or anatomic obstruction of urinary flow at any level of the urinary tract, leading to functional or anatomic renal damage.

Global Renal Functional Changes

• Functional changes associated with obstructive nephropathy include changes in renal hemodynamic variables and glomerular filtration.
• These changes are influenced by the extent and severity of the obstruction, whether unilateral or bilateral, and whether the obstruction persists or has been relieved.

Factors Influencing GFR

• GFR (glomerular filtration rate) is expressed as GFR = Kf (PGC − PT − πGC):
  • Kf: glomerular ultrafiltration coefficient
  • PGC: glomerular capillary pressure (influenced by renal plasma flow (RPF) and arteriolar resistance)
  • PT: hydraulic pressure of fluid in the tubule
  • πGC: oncotic pressure of proteins

Renal Plasma Flow (RPF)

• RPF depends on renal perfusion pressure and intrarenal resistance to flow, primarily mediated by resistances in the afferent and efferent arterioles.
  • RPF = aortic pressure – renal venous pressure – renal vascular resistance
• Obstruction can temporarily or permanently alter GFR and its determinants.

Unilateral vs. Bilateral Ureteral Obstructions

• Unilateral and bilateral ureteral obstructions differ in the patterns of hemodynamic changes, ureteral pressure changes, and distribution of renal blood flow.

Hemodynamic Changes with Unilateral Ureteral Occlusion (UUO)

• UUO demonstrates a triphasic pattern of RBF and ureteral pressure changes:
  • Phase 1 (1-2 hours): Increased RBF and high PT/collecting system pressure.
  • Phase 2 (3-4 hours): Elevated pressure parameters, declining RBF.
  • Phase 3 (5+ hours): Further decline in RBF and decrease in PT/collecting system pressure.

Hemodynamic Changes with Bilateral Ureteral Occlusion (BUO)

• BUO results in a modest increase in RBF lasting about 90 minutes, followed by a prolonged and more significant decline in RBF than in UUO.
• Intrarenal blood flow distribution is different in BUO compared to UUO.
• Ureteral and tubular pressures are elevated for the first 4-5 hours, remain elevated for at least 24 hours with BUO, and approach pre-occlusion levels after 24 hours in UUO.

Summary of UUO and BUO

• Both involve increases in renal vascular resistance and ureteral pressure.
• Timing and regulation differ.
• UUO: initial vasodilation (prostaglandins/NO), followed by prolonged vasoconstriction, and normalization of pressure.
• BUO: little initial vasodilation, more profound vasoconstriction; postobstructive diuresis is greater due to volume expansion, urea, osmolytes, and ANP.

Pathologic Changes of Obstruction

• Pathologic changes are affected by infection presence/duration, and intra/extrarenal localization.

Gross Pathologic Findings

• Findings at varying post-obstruction time points (42 hours, 7 days, 12 days, 21/28 days, 6 weeks) include dilation of the pelvis/ureter, blunting of papillary tips, increased renal weight, edema, cortical enlargement, increased calyceal dilation, and thinned cortex/medullary tissue.

Microscopic Pathologic Findings

• Findings include widespread glomerular collapse and tubular atrophy, interstitial fibrosis, and proliferation of connective tissue in the collecting system (5-6 weeks after obstruction) with a cell-poor stroma composed of elastic and collagen fibers in the renal interstitium in obstructed portions.

Electron Microscopic Pathologic Findings

• Electron microscopy shows tubular atrophy, glomerular collapse, and renal pelvic smooth muscle atrophy.
• Obstructed portions of the collecting system demonstrate other changes, including a cell-poor stroma composed of elastic and collagen fibers.

Post Obstructive Diuresis

• Relief of obstruction results in significant polyuria (urine outputs of 200 mL/hr or greater).
• Occurs primarily in bilateral obstruction (BUO), often self-limiting, and rarely occurs with contralateral normal kidney.

Post Obstructive Diuresis Mechanisms

• Downregulation of sodium transporters contributes to the saline diuresis.
• Increased ANP and other natriuretic peptides play a role.
• Poor responsiveness of collecting duct to ADH (due to downregulation of aquaporin water channels) contributes.

Selected Extrinsic Causes of Ureteral Obstruction

• Retroperitoneal Fibrosis: Fibrotic/inflammatory mass envelops retroperitoneal structures, potentially obstructing ureters.
• Pelvic Lipomatosis: Rare benign condition of pelvic adipose tissue overgrowth, potentially causing ureteral obstruction.

Obstetric and Gynecologic

• Pregnancy: Hydronephrosis is common during pregnancy (43-100% occurrence), often resolving within 6 weeks postpartum; hormonal (progesterone) and mechanical (uterus compression) factors contribute.

Benign Pelvic Abnormalities

• Tubo-ovarian Abscess: Tubo-ovarian abscess, often associated with PID, may cause extrinsic ureteral obstruction, possibly leading to anuria, treatable with antibiotic therapy, transvaginal drainage, open/laparoscopic intervention, internalized ureteral stents or percutaneous nephrostomy.
• Endometriosis: Defined by endometrial tissue in ectopic locations, affects 10-20% of reproductive-age women, peaking in the mid-20s; potential for malignant transformation.

Vascular Obstruction

• Abdominal Aortic Aneurysm (AAA): Signs of AAA may be initial manifestation of ureteral obstruction (due to mass effect or localized inflammation).
  • Ureteral deviation may occur (pushed laterally or medially, with possible obstruction associated with desmoplastic reaction of inflammatory aneurysms or IAAA).
  • Close monitoring is necessary with stent placement or an endovascular approach for possible recurrent or de novo ureteral obstruction.