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Summary Table

Domain	Detail
Risk Factors	Older males (BPH), nephrolithiasis, pregnancy, pelvic/abdominal malignancy, neurogenic bladder, congenital anomalies (UPJ obstruction in neonates), chronic anticholinergic use
Etiology	Obstruction of urinary outflow at any point from the renal pelvis to the urethral meatus, resulting in retrograde pressure and collecting system dilation
Patient Presentation	Flank pain (colicky or dull), decreased urine output or anuria (bilateral obstruction), hematuria, recurrent UTIs; may be entirely asymptomatic and found incidentally
Classic Physical Exam	CVA tenderness, palpable flank mass (severe/chronic cases, neonates), distended suprapubic bladder (lower tract obstruction), signs of uremia if bilateral
Key Diagnostic Results	Renal ultrasound: dilated pelvis and calyces; elevated BUN/creatinine (bilateral or solitary kidney); non-contrast CT to localize the obstructing lesion
Management	Relieve obstruction first: Foley catheter (bladder outlet), ureteral stent or percutaneous nephrostomy (upper tract); treat underlying cause; monitor for post-obstructive diuresis
Keywords	"Dilated collecting system," "post-renal AKI," "backup of urine," "CVA tenderness with rising creatinine," "bilateral hydronephrosis with anuria," "UPJ obstruction in newborn"

1. Pathophysiology

Hydronephrosis is not a primary disease. It is a structural consequence of urinary tract obstruction. The core concept is straightforward: when urine cannot drain, pressure builds behind the blockage, and the collecting system dilates.

Under normal physiology, urine flows from the renal tubules into the calyces, through the renal pelvis, down the ureter via peristalsis, into the bladder, and out the urethra. When any segment of this pathway is blocked, pressure rises proximal to the obstruction. This is the retrograde pressure transmission principle. The renal pelvis and calyces, being compliant structures, distend in response.

The critical pathophysiologic link to understand is what this pressure does to the kidney itself. The net filtration pressure at the glomerulus equals the hydrostatic pressure in the glomerular capillary minus the sum of oncotic pressure and Bowman's capsule pressure:

$$P_{net} = P_{GC} - (\pi_{GC} + P_{BC})$$

When outflow is obstructed, the back-pressure raises $P_{BC}$ (Bowman's capsule pressure), which directly reduces net filtration pressure and lowers GFR. This is why bilateral hydronephrosis (or hydronephrosis in a solitary kidney) causes post-renal AKI with rising creatinine. Unilateral obstruction, by contrast, typically does not raise creatinine because the contralateral kidney compensates fully.

Beyond the hemodynamic effects, sustained elevated pressure compresses the renal medulla first, then the cortex. The medullary structures (loops of Henle, collecting ducts, vasa recta) are damaged early, which destroys the medullary concentration gradient. This explains a finding that often surprises students: patients with chronic bilateral obstruction may actually present with polyuria and dilute urine rather than oliguria. The kidneys lose their concentrating ability before they lose overall filtration.

Prolonged obstruction triggers tubular atrophy, interstitial fibrosis, and irreversible nephron loss. The general clinical teaching is that obstruction persisting beyond 12 to 14 days carries a substantially higher risk of permanent damage, though partial recovery can occur even after longer durations if decompression is performed.

When obstruction coexists with infection, the stagnant urine creates an ideal bacterial growth medium. This condition, known as pyonephrosis (infected hydronephrosis), is a urologic emergency. The obstructed, infected kidney behaves as a closed-space abscess. Antibiotics cannot adequately penetrate, and drainage is mandatory. This concept is tested frequently.

2. Classification and Clinical Manifestation

Classification by Level of Obstruction

Level	Common Causes	Typical Laterality
Renal pelvis / Ureteropelvic junction (UPJ)	UPJ obstruction (most common congenital cause), renal calculi, blood clots, papillary necrosis fragments	Unilateral
Ureter	Ureteral calculi (most common overall cause in young adults), ureteral stricture, extrinsic compression (tumor, retroperitoneal fibrosis, gravid uterus)	Unilateral or bilateral
Bladder	Neurogenic bladder, bladder carcinoma, bladder calculi	Bilateral
Urethra / Bladder outlet	BPH (most common cause in older males), urethral stricture, posterior urethral valves (most common cause of bilateral hydronephrosis in male neonates)	Bilateral

Grading by Severity (Society for Fetal Urology Ultrasound Grading)

Grade	Ultrasound Appearance	Clinical Significance
Grade 0	No dilation	Normal
Grade I (Mild)	Renal pelvis mildly dilated only; calyces not affected	Often physiologic (especially in pregnancy); usually observation
Grade II (Mild to Moderate)	Pelvis dilated with extension into major calyces	Warrants further workup for a cause
Grade III (Moderate)	Pelvis and all calyces uniformly dilated; parenchyma preserved	Likely obstructive; evaluate for intervention
Grade IV (Severe)	All calyces ballooned with thinning of renal parenchyma	High risk of irreversible damage; urgent decompression typically required

Clinical Manifestation by Acuity

Feature	Acute Obstruction	Chronic Obstruction
Pain	Severe colicky flank pain radiating to the groin (classic renal colic)	Dull, vague flank ache or completely painless
Urine output	Sudden oliguria or anuria (bilateral)	Paradoxical polyuria (loss of concentrating ability), nocturia
Systemic signs	Nausea, vomiting, diaphoresis	Hypertension (renin-angiotensin activation), progressive CKD features
Infection signs	Fever, rigors, sepsis if pyonephrosis develops	Recurrent UTIs
Renal function	Acute creatinine elevation (bilateral)	Gradual, insidious decline; may present as unexplained CKD
Physical exam	Marked CVA tenderness	Palpable flank mass possible; may have no focal findings

3. Diagnostic Workup

Test	Role	Key Findings
Renal Ultrasound	Best initial test	Dilated renal pelvis/calyces; assess parenchymal thickness; evaluate bladder distension
Non-contrast CT Abdomen/Pelvis	Best test to identify the obstructing lesion (especially calculi)	Location, size, and nature of obstruction; perinephric stranding; sensitivity >95% for stones
BUN / Creatinine	Assess functional impact on kidneys	Elevated in bilateral obstruction or solitary kidney
Urinalysis + Culture	Screen for infection and hematuria	Pyuria/bacteriuria indicate infected system; hematuria suggests stones
CBC	Evaluate for systemic infection	Leukocytosis with left shift in pyonephrosis
Basic Metabolic Panel	Monitor electrolytes	Hyperkalemia, non-anion-gap metabolic acidosis (type IV RTA pattern)
Post-void Residual (PVR)	Assess for bladder outlet obstruction	PVR >200 mL indicates incomplete emptying
Diuretic Renography (MAG3 scan)	Confirmatory test for functional obstruction (especially UPJ obstruction)	Plateau or rising curve after furosemide = true obstruction; prompt washout = non-obstructive dilation
VCUG	Evaluate vesicoureteral reflux, posterior urethral valves	Contrast refluxing into ureters; dilated posterior urethra in PUV

The best initial test for suspected hydronephrosis is a renal ultrasound. It is noninvasive, requires no radiation, is inexpensive, and has high sensitivity for detecting collecting system dilation. Ultrasound answers the single most important initial question: is the collecting system dilated or not? It also provides information about parenchymal thickness, which helps distinguish acute from chronic obstruction. In pregnancy, ultrasound is the unquestioned first-line modality.

The main limitation of ultrasound is that it shows you the consequence (dilation) without reliably showing you the cause. The mid-ureter is notoriously difficult to visualize due to overlying bowel gas. For this reason, non-contrast CT of the abdomen and pelvis is the next step when the cause must be identified, particularly when nephrolithiasis is suspected. Non-contrast CT has greater than 95% sensitivity and nearly 100% sensitivity for ureteral stones and is excellent at demonstrating the level of obstruction, secondary signs of acute obstruction (perinephric fat stranding, periureteral edema), and alternative pathology such as tumors or retroperitoneal fibrosis. The reason contrast is withheld initially is twofold: IV contrast can obscure radiopaque stones and carries nephrotoxicity risk in a patient whose renal function may already be compromised.

Laboratory evaluation is essential to assess functional impact. BUN and creatinine establish whether renal function is compromised. If creatinine is elevated in the setting of bilateral hydronephrosis, the diagnosis is post-renal AKI, and the urgency of decompression increases. Electrolytes should be checked because obstructive uropathy damages distal tubular function, impairing potassium and acid secretion, producing a type IV RTA pattern (hyperkalemia with non-anion-gap metabolic acidosis).

Urinalysis and urine culture are non-negotiable. The combination of hydronephrosis, fever, and pyuria points toward pyonephrosis, which changes the management algorithm from "urgent" to "emergent." This is a point where exam questions test whether you recognize the need for drainage over antibiotics alone.

For cases where the clinical question is whether dilation represents true obstruction or simply a floppy, non-obstructed system (common in congenital anomalies and prenatal findings), diuretic renography (MAG3 scan with furosemide) is the confirmatory functional test. A radiotracer is injected, and its clearance from the kidney is measured. Furosemide is then administered. If the tracer washes out briskly, the system is not truly obstructed. If the tracer shows a plateau or rising curve, functional obstruction is confirmed. This test is particularly important in the workup of UPJ obstruction in children, where the decision to proceed with pyeloplasty rests on demonstrating functional compromise.

4. Management & Treatment

Clinical Scenario	Intervention	Details
Bladder outlet obstruction	Foley catheter	Immediate decompression; monitor for post-obstructive diuresis
Upper tract obstruction, stable patient	Ureteral stent (double-J)	Placed cystoscopically; bypasses the point of obstruction
Upper tract obstruction, stent not feasible	Percutaneous nephrostomy (PCN)	IR-guided tube directly into the renal pelvis
Infected hydronephrosis / Pyonephrosis	Emergent drainage (PCN or stent) + IV antibiotics	Drainage is the priority; antibiotics alone will fail
Obstructing ureteral stone < 10 mm	Medical expulsive therapy	Tamsulosin 0.4 mg PO daily + analgesics; observe for 4 to 6 weeks
Obstructing stone > 10 mm or failed passage	Surgical stone removal	Ureteroscopy with laser lithotripsy, shock wave lithotripsy (SWL), or PCNL for large renal stones
BPH causing chronic obstruction	Alpha-blocker + 5-alpha-reductase inhibitor	Tamsulosin 0.4 mg daily + finasteride 5 mg daily; TURP if refractory
UPJ obstruction	Pyeloplasty	Surgical reconstruction of the UPJ; definitive treatment
Malignant obstruction	Stent or PCN + treat the malignancy	Stents may need periodic exchange
Post-obstructive diuresis	Fluid replacement + electrolyte monitoring	Replace 50 to 75% of urine output with NS; check lytes every 6 to 12 hours

Step 1: Decompress the obstructed system. This is the "next best step" in virtually every exam question involving hydronephrosis with compromised renal function. The instinct being tested is: relieve the obstruction first, investigate the cause second. For lower tract obstruction (e.g., BPH, urethral stricture), the immediate intervention is a Foley catheter. For upper tract obstruction where a catheter will not help, the choice is between a retrograde ureteral stent (placed by urology via cystoscopy) or an antegrade percutaneous nephrostomy (placed by interventional radiology). The choice between these depends on clinical context, operator availability, and patient anatomy.

Step 2: Address infection with drainage, not just antibiotics. If fever, pyuria, and a positive culture accompany hydronephrosis, you are dealing with pyonephrosis. Start broad-spectrum IV antibiotics immediately (piperacillin-tazobactam 3.375 g IV every 6 hours, or meropenem 1 g IV every 8 hours if resistant organisms are suspected). However, the non-negotiable teaching point is that antibiotics without drainage will fail. The obstructed infected kidney functions as a walled-off collection that antibiotics cannot adequately penetrate. Emergent drainage via nephrostomy or stent is required. This is a frequently tested "next best step" question where students choose antibiotics alone and get it wrong.

Step 3: Treat the underlying cause. Once acute decompression is achieved, definitive management targets the root pathology:

For nephrolithiasis, stones smaller than 10 mm in the distal ureter have a reasonable chance of spontaneous passage. Medical expulsive therapy with tamsulosin 0.4 mg orally once daily (an alpha-1 blocker that relaxes ureteral smooth muscle) is given alongside adequate analgesia (ketorolac 15 to 30 mg IV, or ibuprofen 400 to 600 mg PO every 6 to 8 hours). If the stone has not passed in 4 to 6 weeks, or if it is larger than 10 mm, or if the patient develops infection, intractable pain, or worsening renal function, surgical intervention is indicated. Options include ureteroscopy with laser lithotripsy (preferred for mid and distal ureteral stones), shock wave lithotripsy (preferred for proximal ureteral or renal stones < 2 cm), and percutaneous nephrolithotomy (for renal stones > 2 cm or staghorn calculi).

For BPH, long-term medical therapy combines an alpha-blocker (tamsulosin 0.4 mg daily) with a 5-alpha-reductase inhibitor (finasteride 5 mg daily). Finasteride reduces prostate volume over 6 to 12 months by blocking the conversion of testosterone to dihydrotestosterone. If medical therapy fails or the patient develops refractory urinary retention, recurrent UTIs, or persistent hydronephrosis, TURP (transurethral resection of the prostate) is the surgical standard.

For UPJ obstruction, the definitive treatment is pyeloplasty, a surgical reconstruction that excises the obstructed segment and re-anastomoses the ureter to the renal pelvis. In pediatric patients, the decision to operate is guided by diuretic renography results (demonstrating functional obstruction and differential renal function).

Step 4: Manage post-obstructive diuresis. This is a critical and frequently tested complication. After decompression of chronic bilateral obstruction, patients often produce enormous volumes of urine (sometimes exceeding 500 mL/hour). The mechanism involves multiple factors: accumulated urea acts as an osmotic diuretic, the damaged medullary interstitium cannot concentrate urine, and volume overload from the period of obstruction is being corrected. The danger lies in rapid volume depletion, hyponatremia, and hypokalemia if the diuresis is not managed carefully.

The correct approach is to replace approximately 50 to 75% of hourly urine output with intravenous normal saline. Matching output milliliter-for-milliliter is a trap answer because it perpetuates the diuresis by maintaining the volume stimulus. Electrolytes (particularly potassium and sodium) should be checked every 6 to 12 hours. The diuresis typically resolves within 24 to 48 hours as renal function stabilizes.

Contraindications and Special Populations: In pregnancy, imaging should be limited to ultrasound. MRI without gadolinium is an acceptable second-line modality. CT is avoided unless no other option exists. Physiologic hydronephrosis of pregnancy (predominantly right-sided due to uterine dextrorotation and compression by the right ovarian vein) must be differentiated from pathologic obstruction. For intervention, ureteral stenting is generally preferred over nephrostomy when feasible.

In patients with coagulopathy, percutaneous nephrostomy carries increased bleeding risk. Correct coagulopathy before the procedure or opt for retrograde stenting if possible.

5. Differential Diagnosis & Distractors

Differential	Why It Is Similar	Key Discriminator
Physiologic hydronephrosis of pregnancy	Bilateral (right-predominant) dilation of the collecting system during second/third trimester	No pain, no elevated creatinine, resolves postpartum; right side more affected; no identifiable obstructing lesion
Simple renal cyst	Both appear as fluid-filled structures on ultrasound	A cyst is a discrete, round, anechoic structure that does not communicate with the collecting system; hydronephrosis shows a branching pelvicalyceal dilation pattern
Parapelvic cyst	Located at the renal hilum; can closely mimic a dilated renal pelvis	Does not connect with the collecting system on CT urography or contrast-enhanced studies
Vesicoureteral reflux (VUR)	Can cause bilateral hydroureteronephrosis, especially in pediatric patients	Dilation is caused by retrograde urine flow, not antegrade obstruction; diagnosed by VCUG showing contrast refluxing upward during voiding
Acute pyelonephritis	Both present with flank pain, fever, and CVA tenderness	Pyelonephritis does not cause collecting system dilation unless concurrent obstruction exists; urinalysis shows WBC casts; imaging shows renal parenchymal inflammation without pelvic dilation
Renal cell carcinoma	Can cause hydronephrosis if the tumor obstructs the pelvis or ureter	Imaging reveals a solid, enhancing renal mass; hematuria is painless and often gross; constitutional symptoms (weight loss, night sweats) may be present
Retroperitoneal fibrosis	Causes bilateral hydronephrosis by encasing the ureters	CT demonstrates a fibrotic soft-tissue mass surrounding the aorta at L4-L5; ureters are characteristically pulled medially (not displaced laterally)
Multicystic dysplastic kidney (MCDK)	In neonates, both present as a large, cystic renal mass on prenatal or postnatal ultrasound	MCDK shows multiple non-communicating cysts of varying sizes with no identifiable renal pelvis; hydronephrosis shows a central dilated pelvis communicating with dilated calyces

6. Traps & High-Yield Pearls

The most common trap involving hydronephrosis on licensing exams is failing to identify post-renal obstruction as the cause of acute kidney injury. When a vignette presents rising creatinine with oliguria or anuria, students often focus on intrinsic renal etiologies (ATN, glomerulonephritis) and order tests like renal biopsy or urine eosinophils. The correct first step is a renal ultrasound to rule out obstruction. Post-renal AKI is the most readily reversible cause of kidney injury, and the exam rewards the student who thinks of it first.

The second classic trap is the pyonephrosis management question. The vignette will describe a patient with hydronephrosis, fever, and pyuria. The distractors will include "start IV antibiotics and reassess in 48 hours." This answer is wrong. Antibiotics alone cannot treat a closed infected space. The answer is always emergent drainage plus antibiotics. If you remember only one thing about infected hydronephrosis, remember that drainage is non-negotiable.

Third, beware of pregnancy-related confusion. A mild right-sided hydronephrosis found incidentally in a 28-week pregnant woman with no symptoms and normal creatinine is almost certainly physiologic. Do not order CT. Do not recommend stenting. The answer is observation.

Fourth, the post-obstructive diuresis question is a classic trap. After relief of chronic bilateral obstruction, the patient makes enormous amounts of dilute urine. The wrong answer is to match output 1:1 with IV fluids. The correct approach is to replace 50 to 75% of output with normal saline and check electrolytes every 6 to 12 hours. Matching output fully perpetuates the diuresis, while ignoring it entirely risks hypovolemic shock.

Finally, students sometimes confuse hydronephrosis with a parapelvic cyst or a multicystic dysplastic kidney. The key is communication: in hydronephrosis, the dilated calyces connect with a dilated pelvis in a recognizable branching pattern. In cystic conditions, the fluid collections are isolated and do not interconnect. This distinction is often presented as an ultrasound image interpretation question.

The core competency being assessed across all hydronephrosis questions is the ability to recognize obstruction as a cause of renal dysfunction, image it correctly, decompress it urgently, and manage the physiologic consequences of relief.

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