Hydronephrosis

Introduction

Hydronephrosis describes dilatation of the renal pelvis and calyces. It is important to be clear that this is a descriptive radiological finding rather than a diagnosis in itself - the clinical work lies in establishing whether there is true obstruction, where that obstruction is, what is causing it, and whether renal function is threatened.¹

Sustained obstruction raises pressure within the collecting system, which is transmitted back to the nephron. This reduces glomerular filtration, causes progressive tubular atrophy and interstitial fibrosis, and ultimately produces cortical thinning and irreversible loss of function. The rate at which this happens is the reason obstruction is treated urgently: significant damage can begin within days to weeks, and a chronically obstructed kidney may never recover useful function.

Causes

Causes are conventionally divided by their relationship to the wall of the urinary tract, which is a reliable way to structure an answer.

Clinical features

Presentation depends entirely on how quickly the obstruction developed, whether it is unilateral or bilateral, and whether infection is present. Chronic, gradual obstruction is often silent until function is substantially lost.

Acute obstruction

• Severe colicky loin pain - rapid distension of the collecting system, typically from a stone
• Nausea and vomiting
• Haematuria
• Restlessness - the patient cannot lie still

Chronic obstruction

• Often completely asymptomatic, discovered incidentally on imaging performed for another reason
• Dull, persistent loin ache rather than colic, sometimes worse after drinking large volumes (classically in PUJ obstruction, 'Dietl's crisis')
• A palpable flank mass in gross hydronephrosis
• Recurrent urinary tract infections from stasis
• Insidious features of chronic kidney disease - fatigue, nausea, anaemia, hypertension

Features pointing to the underlying cause

• Lower urinary tract symptoms - hesitancy, poor stream, terminal dribbling, incomplete emptying, nocturia: suggests bladder outlet obstruction, usually prostatic in men
• Acute urinary retention with a painful, palpable bladder
• Anuria or marked oliguria - implies complete bilateral obstruction (or obstruction of a solitary kidney) and is a medical emergency
• Fever and rigors - infection above the obstruction; an emergency
• Weight loss, haematuria, bone pain or a pelvic mass - suggests malignancy
• Antenatal detection - hydronephrosis is one of the commonest findings on the routine 20-week anomaly scan, and prompts postnatal assessment for PUJ obstruction, vesicoureteric reflux or posterior urethral valves

Investigations

Imaging

• Renal tract ultrasound - first line. It confirms hydronephrosis, grades its severity, assesses cortical thickness (thinning indicating chronicity and lost function), and shows bladder volume. It is quick, safe and radiation-free, making it the test of choice in pregnancy and children. Its weakness is that it cannot reliably identify the cause or the level of obstruction, and it may miss obstruction in a dehydrated patient or in retroperitoneal fibrosis, where the ureters are encased and cannot dilate
• Bladder scan (post-void residual) - simple, immediate, and essential: a large residual volume points to bladder outlet obstruction and means the first treatment is a catheter
• Non-contrast CT KUB - excellent for stones and for defining the level of obstruction
• CT with contrast / CT urogram - to characterise masses, retroperitoneal fibrosis and urothelial tumours
• MAG3 or DTPA renography (nuclear medicine) - the definitive test to distinguish obstructive from non-obstructive dilatation and to quantify differential function between the two kidneys. This determines whether a poorly functioning, chronically obstructed kidney is worth salvaging
• DMSA scan - assesses renal scarring and split function, particularly in children
• Micturating cystourethrogram (MCUG) - in infants and children to demonstrate vesicoureteric reflux or posterior urethral valves
• Antegrade or retrograde pyelography - defines the level of obstruction precisely, often performed at the time of stenting or nephrostomy

Laboratory

• U&Es and creatinine - to identify AKI and establish baseline function. Remember that these are often normal in unilateral obstruction
• FBC and CRP - evidence of infection
• Urine dipstick and culture - haematuria suggesting stones or tumour; nitrites and leucocytes suggesting infection
• Blood cultures if febrile
• Venous blood gas - for rapid potassium in AKI, and to assess acidosis
• PSA in men with suspected prostatic obstruction (interpreting with caution, as retention and catheterisation raise it)
• Calcium, urate and stone screen where calculi are the cause
• ESR, CRP and autoimmune screen if retroperitoneal fibrosis is suspected; IgG4 levels may be relevant

Management

Management has three components in sequence: decide whether decompression is urgent, relieve the obstruction at the appropriate level, and then treat the underlying cause.

Urgent decompression

Immediate relief of obstruction is required where there is infection, acute kidney injury, a solitary or transplanted kidney, bilateral obstruction, or intractable pain.

Treating the underlying cause

• Stones - ureteroscopy, lithotripsy or PCNL once any sepsis has settled
• Benign prostatic hyperplasia - alpha-blockers and 5-alpha reductase inhibitors, with TURP for those failing medical therapy or with high-pressure chronic retention
• Malignancy - oncological management, with stenting or nephrostomy for palliation of obstruction
• PUJ obstruction - pyeloplasty, where function is worth preserving
• Retroperitoneal fibrosis - corticosteroids, sometimes with other immunosuppression, plus stenting or ureterolysis
• Posterior urethral valves - endoscopic valve ablation in infancy
• Vesicoureteric reflux - antibiotic prophylaxis and surveillance in children, with surgery in selected cases
• Nephrectomy - considered for a chronically obstructed, non-functioning kidney that is causing pain, infection or hypertension

Complications

• Acute kidney injury - particularly with bilateral obstruction or a solitary kidney
• Chronic kidney disease and end-stage renal disease - from sustained obstruction causing tubular atrophy, interstitial fibrosis and cortical thinning
• Irreversible loss of the affected kidney - the risk rises steeply the longer obstruction persists
• Infection: pyelonephritis, pyonephrosis and urosepsis - stasis strongly predisposes to infection, and an infected obstructed system is life-threatening
• Stone formation - stasis promotes crystallisation, creating a self-perpetuating cycle
• Hypertension - from activation of the renin-angiotensin-aldosterone system in the obstructed kidney
• Post-obstructive diuresis with dehydration and electrolyte disturbance
• Renal tubular acidosis and hyperkalaemia - impaired distal tubular function in chronic obstruction
• Spontaneous rupture of the collecting system - rare, with acute severe obstruction
• Complications of intervention - stent discomfort, encrustation, migration and infection; bleeding after nephrostomy

Red flags

Prognosis

Prognosis is determined almost entirely by the duration and completeness of obstruction, and by whether infection supervenes. Acute obstruction relieved within a few days is generally followed by full recovery of renal function. Beyond a few weeks, recovery becomes progressively less complete, and obstruction persisting for months typically leaves permanent loss of function in that kidney.

Cortical thickness on ultrasound and differential function on MAG3 renography are the practical guides to salvageability. A kidney with preserved cortex and reasonable split function is worth decompressing and reconstructing; one with a thin cortex contributing very little function may be better managed conservatively or, if it is causing pain, infection or hypertension, by nephrectomy.

Unilateral obstruction with a healthy contralateral kidney rarely causes renal failure, because the normal kidney compensates - which is precisely why it can progress silently to complete loss of the affected side with an entirely normal creatinine throughout. Bilateral obstruction, by contrast, presents earlier with AKI but is frequently and dramatically reversible: relieving bladder outlet obstruction with a catheter can return a severely uraemic patient to near-normal function within days. In children, the long-term outlook depends on the underlying anomaly, with posterior urethral valves carrying the greatest risk of progressive chronic kidney disease despite early intervention.