Renal: Tubular Inherited Stones (Complete)

• Acid–base and tubules: Acid–Base Made Simple | Renal Tubular Acidosis | Hypokalaemia | Magnesium and Phosphate | Inherited Tubular Syndromes | Chronic Interstitial Nephritis
• Inherited kidney disease: Polycystic Kidney Disease (ADPKD) | Alport Syndrome | Fabry Disease | Other Inherited and Cystic Conditions
• Urinary tract and pregnancy: Kidney Stones | Renal Colic | Preventing Stones | Lower Urinary Tract Infection | UTI in Special Groups | Pyelonephritis | Chronic Obstruction and Hydronephrosis | The Kidney in Pregnancy
• Revision: Drug Reference Table | Spot the Diagnosis | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🫘 Tubular disorders, inherited kidney disease, stones and infection — the tubules fine-tune acid, potassium, magnesium and phosphate, and their disorders are favourite exam topics. Inherited diseases like ADPKD and Alport syndrome are common causes of kidney failure in young adults. Stones and UTIs are among the most common reasons people see a doctor about their kidneys.
Your four questions for every patient: What do the gas, anion gap and potassium tell me? Is there a family history that points to an inherited disease? Is there obstruction or infection that needs urgent action? Is the patient pregnant (it changes the normal ranges, drugs and risks)?

Acid–Base Made Simple

Step by step:

• 1. pH — under 7.35 is acidaemia; over 7.45 is alkalaemia.
• 2. Primary problem:
  • Low bicarbonate (under 22) = metabolic acidosis.
  • High pCO2 (over 6.0 kPa) = respiratory acidosis.
  • High bicarbonate (over 26) = metabolic alkalosis.
  • Low pCO2 (under 4.7 kPa) = respiratory alkalosis.
• 3. Compensation — in metabolic acidosis, expected pCO2 (kPa) ≈ (0.2 × HCO3) + 1.1 (Winter's formula). Higher than expected means an added respiratory acidosis.
• 4. Anion gap (in metabolic acidosis) = Na − (Cl + HCO3); normal about 8–12 (lower if albumin is low).

• Osmolar gap (measured minus calculated osmolality; calculated = 2Na + urea + glucose) over about 10 suggests toxic alcohols (methanol, ethylene glycol).
• Urine anion gap (Na + K − Cl) in normal anion gap acidosis:
  • Negative — kidneys are excreting acid normally (diarrhoea).
  • Positive — kidneys can't excrete acid (renal tubular acidosis).
• Metabolic alkalosis — urine chloride under 20 mmol/L suggests volume depletion (vomiting) that responds to saline; over 20 suggests mineralocorticoid excess or current diuretics.

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Renal Tubular Acidosis

What it is: A normal anion gap metabolic acidosis because the tubules can't handle acid or bicarbonate properly, with a near-normal GFR.

• Treatment:
  • Type 1 — potassium citrate or sodium bicarbonate (moderate doses); corrects acidosis, potassium and stone risk.
  • Type 2 — large doses of bicarbonate or citrate (bicarbonate is lost as fast as it's given); potassium; vitamin D and phosphate for bone disease.
  • Type 4 — stop culprit drugs; low-potassium diet; loop or thiazide diuretic; potassium binders; fludrocortisone if there is no hypertension or fluid overload.

💡 Clinical Pearl: Distal (type 1) RTA = stones and a high urine pH. Proximal (type 2) RTA = bone disease and Fanconi syndrome. Type 4 = high potassium, usually from diabetes or drugs.

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Hypokalaemia

• Severity: Mild 3.0–3.4; moderate 2.5–2.9; severe under 2.5 mmol/L or with symptoms or ECG changes.
• Causes:
  • GI loss — diarrhoea, vomiting, laxatives, high-output stoma.
  • Renal loss:
    • Diuretics (loop and thiazide).
    • Hyperaldosteronism (Conn's), Cushing's, liquorice.
    • Renal tubular acidosis (types 1 and 2).
    • Bartter and Gitelman syndromes.
    • Low magnesium.
    • Amphotericin.
  • Shift into cells — insulin, salbutamol, theophylline, alkalosis, refeeding, thyrotoxic periodic paralysis.
  • Poor intake (rarely alone).
• Features:
  • Weakness, cramps, constipation, ileus.
  • Arrhythmias (worse with digoxin or heart disease).
  • Polyuria (nephrogenic DI).
  • ECG: Flat T waves, U waves, ST depression, long QT.
• Tests if unexplained: magnesium, bicarbonate (alkalosis vs acidosis), BP, renin and aldosterone, urine potassium.
• Treatment:
  • Mild to moderate — oral potassium chloride (e.g. Sando-K 2 tablets two to three times daily, about 24 mmol per 2 tablets); potassium-sparing diuretic if from ongoing diuretic use.
  • Severe or symptomatic — IV potassium chloride in pre-mixed bags:
    • Peripheral line — usually no faster than 10 mmol/hour.
    • Faster rates (up to 20 mmol/hour or more) only via a central line with cardiac monitoring (local protocol).
    • Never give undiluted potassium as a bolus.
  • Correct magnesium — hypokalaemia won't correct while magnesium is low.
  • Treat the cause.

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Magnesium and Phosphate

• Low magnesium (under 0.7 mmol/L):
  • Causes — PPIs (long-term), diuretics, alcohol, diarrhoea, high-output stoma, refeeding, Gitelman syndrome, cisplatin, calcineurin inhibitors.
  • Features — tremor, cramps, tetany, seizures, arrhythmias (torsades de pointes), resistant low potassium and low calcium (low magnesium blocks PTH release).
  • Treatment:
    • Oral — magnesium glycerophosphate or aspartate (diarrhoea limits the dose).
    • IV — magnesium sulfate, e.g. 20 mmol over 2–4 hours (faster — 2 g over 10–15 minutes — for torsades or seizures).
    • Reduce the dose in kidney impairment.
• High magnesium — kidney failure, magnesium infusions (pre-eclampsia), laxatives or antacids: loss of reflexes, low BP, breathing depression, heart block. Stop magnesium; IV calcium gluconate; dialysis if severe.
• Low phosphate (under 0.8 mmol/L; severe under 0.32):
  • Causes:
    • Refeeding syndrome.
    • Alcohol.
    • Treatment of DKA.
    • Primary hyperparathyroidism; vitamin D deficiency.
    • Fanconi syndrome.
    • IV iron (especially ferric carboxymaltose — raises FGF-23).
    • FGF-23 excess — X-linked hypophosphataemia (treated with burosumab), tumour-induced osteomalacia.
    • Phosphate binders, antacids.
  • Features (when severe) — muscle weakness, breathing failure (hard to wean from ventilators), heart failure, rhabdomyolysis, haemolysis, confusion; osteomalacia if chronic.
  • Treatment — oral phosphate (e.g. Phosphate Sandoz) or IV phosphate for severe or symptomatic cases (watch calcium).
• High phosphate — CKD, tumour lysis syndrome, rhabdomyolysis, phosphate enemas; treated with binders, diet and dialysis (see the CKD chapter).

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Inherited Tubular Syndromes

💡 Clinical Pearl: Low potassium and alkalosis: check BP and renin/aldosterone. Normal BP suggests diuretics, vomiting, Bartter or Gitelman (check urine calcium and magnesium). High BP with high aldosterone suggests Conn's; with low aldosterone suggests Liddle, liquorice or Cushing's.

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Chronic Interstitial Nephritis

• What it is: Slow scarring of the kidney tissue around the tubules. The urine is often "bland" — little blood, mild (tubular) proteinuria — with tubular problems such as acidosis and polyuria.
• Causes:
  • Lithium — nephrogenic DI and slowly progressive CKD. Check U&E and lithium levels every 3–6 months; discuss alternatives if eGFR falls.
  • Reflux nephropathy — scarring from childhood vesicoureteric reflux and infections; hypertension, proteinuria.
  • Long-term analgesics (NSAIDs; phenacetin historically).
  • Sarcoidosis — granulomatous interstitial nephritis, plus high calcium and stones.
  • Sjögren's syndrome (with type 1 RTA).
  • IgG4-related disease.
  • Lead; aristolochic acid (some herbal remedies).
  • Chronic obstruction.
  • Sickle cell disease; myeloma.
  • ADTKD (inherited — see below).
• Papillary necrosis — the tips of the medullary pyramids die and can slough off, causing colic, haematuria and obstruction. Causes: diabetes, analgesics, sickle cell disease, severe pyelonephritis, obstruction.

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Polycystic Kidney Disease (ADPKD)

• What it is: Autosomal dominant polycystic kidney disease — the commonest inherited kidney disease (about 1 in 1,000 people), causing about 1 in 10 cases of kidney failure.
• Genes:
  • PKD1 (chromosome 16, about 80%) — more severe; kidney failure on average in the mid-50s.
  • PKD2 (chromosome 4) — milder; kidney failure later (often 70s) or not at all.
• Kidney features:
  • Hypertension — often the first sign, in young adults.
  • Loin or back pain; large, palpable kidneys.
  • Visible haematuria (cyst bleeding).
  • Cyst infection; UTIs; stones.
  • Slowly falling eGFR (usually from the 30s–40s).
• Outside the kidneys:
  • Liver cysts — the commonest; can cause a very large liver (worse in women; oestrogen).
  • Intracranial ("berry") aneurysms — about 8–10%; higher with a family history of aneurysm or subarachnoid haemorrhage.
  • Mitral valve prolapse.
  • Hernias; diverticular disease.
  • Pancreatic cysts.
• Diagnosis:
  • Ultrasound in someone with a family history — age-based cyst counts, e.g. 3 or more cysts in total at age 15–39; 2 or more in each kidney at 40–59; 4 or more in each kidney at 60 or over.
  • MRI — more sensitive; measures total kidney volume (predicts progression).
  • Genetic testing — when imaging is unclear, there is no family history, or for assessing a living donor.
• Management:
  • BP control — ACE inhibitor or ARB; lower targets (e.g. 110/75 or below in younger patients with good eGFR, as per the HALT-PKD trial).
  • Drink plenty of water (about 3 L/day) to suppress ADH; low salt; healthy weight.
  • Tolvaptan (vasopressin V2 receptor blocker) — NICE TA358: for CKD stage 2–3 at the start of treatment with evidence of rapidly progressing disease.
    • Slows cyst growth and loss of eGFR.
    • Side effects: thirst and large urine volumes (several litres a day).
    • Liver toxicity — check LFTs monthly for 18 months, then every 3 months.
  • Pain — paracetamol; avoid long-term NSAIDs; cyst drainage or nephrectomy for severe pain.
  • Cyst infection — antibiotics that penetrate cysts (e.g. ciprofloxacin, co-trimoxazole), often for several weeks.
  • Aneurysm screening — MR angiography if there is a family history of aneurysm or SAH, or a high-risk job (e.g. pilots).
  • Family screening after counselling (ultrasound from age 18–20, or genetic testing).
  • Transplant or dialysis for kidney failure; very large kidneys may need removal to make room for a transplant.
• ARPKD (autosomal recessive) — presents in babies and children: very large kidneys, congenital hepatic fibrosis (portal hypertension), lung hypoplasia in severe cases.

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Alport Syndrome

• What it is: Inherited faults in type IV collagen (COL4A3, COL4A4, COL4A5) in the glomerular basement membrane, ear and eye.
• Inheritance:
  • X-linked (COL4A5) — most common; males are severely affected; female carriers often have haematuria and can develop CKD.
  • Autosomal recessive (severe) and autosomal dominant (milder; overlaps with "thin basement membrane disease").
• Features:
  • Haematuria from childhood, then proteinuria, hypertension and progressive CKD (kidney failure often in early adulthood in X-linked males).
  • Sensorineural deafness (high frequency).
  • Eye — anterior lenticonus (cone-shaped lens), dot-and-fleck retinopathy.
• Diagnosis: Genetic testing; biopsy shows a split, "basket-weave" basement membrane on electron microscopy.
• Treatment:
  • Early ACE inhibitor (delays kidney failure); SGLT2 inhibitor.
  • Hearing aids.
  • Transplant — note that some patients develop anti-GBM disease against the "new" normal collagen in the graft.
  • Family screening and genetic counselling.

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Fabry Disease

• What it is: An X-linked lysosomal storage disease — deficiency of alpha-galactosidase A lets a fat (Gb3) build up in blood vessels, kidneys, heart and nerves.
• Features:
  • Burning pain in the hands and feet (acroparaesthesia) from childhood, often with fever or exercise.
  • Angiokeratomas — small dark red spots, often between the umbilicus and knees.
  • Reduced sweating; heat intolerance.
  • Corneal whorls (cornea verticillata).
  • GI pain and diarrhoea.
  • Kidney — proteinuria, CKD from the 30s–40s.
  • Heart — left ventricular hypertrophy, arrhythmias.
  • Early stroke.
  • Women can be affected (often more mildly).
• Diagnosis:
  • Men — low enzyme activity in blood.
  • Women — GLA gene testing (enzyme can be normal).
  • Lyso-Gb3 in blood; "zebra bodies" on electron microscopy of a biopsy.
• Treatment (specialist centres):
  • Enzyme replacement therapy — agalsidase alfa or beta, or pegunigalsidase alfa (IV infusions every 2 weeks).
  • Migalastat (oral "chaperone") — for people with suitable gene variants.
  • ACE inhibitor for proteinuria; pain control.
• Consider it in young people with unexplained CKD, LVH or stroke.

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Other Inherited and Cystic Conditions

• Simple kidney cysts — very common with age; thin-walled, fluid-filled; usually harmless. Complex cysts (thick walls, septa, solid parts) need further imaging (Bosniak classification) because of cancer risk.
• Tuberous sclerosis complex (autosomal dominant):
  • Angiomyolipomas — can bleed (sudden loin pain and shock); everolimus or embolisation for large ones.
  • Kidney cysts.
  • Epilepsy, learning disability.
  • Ash-leaf macules, facial angiofibromas, shagreen patches.
  • Lymphangioleiomyomatosis (LAM) in women.
• Von Hippel–Lindau disease (autosomal dominant):
  • Kidney cysts and clear cell kidney cancer (often multiple).
  • Haemangioblastomas (brain, spine, retina).
  • Phaeochromocytoma.
  • Regular screening; belzutifan for associated tumours.
• Autosomal dominant tubulointerstitial kidney disease (ADTKD) — e.g. UMOD (uromodulin) variants: early gout, bland urine, slowly progressive CKD, strong family history.
• Medullary sponge kidney — dilated collecting ducts (usually not inherited): stones, nephrocalcinosis, UTIs, haematuria; good kidney function.
• APOL1 kidney disease — gene variants in people of West African ancestry raise the risk of FSGS, hypertensive-type CKD and HIVAN.
• Primary hyperoxaluria — rare; recurrent calcium oxalate stones and nephrocalcinosis from childhood; lumasiran (RNA therapy) for type 1.
• Cystinosis — lysosomal disease: Fanconi syndrome in infancy; cysteamine.
• Genetic testing — the NHS Genomic Medicine Service offers panels for unexplained kidney failure in young people, family history, and cystic disease.

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Kidney Stones

• How common: About 1 in 10 people in their lifetime; peak age 30–60; more men; about half have another stone within 5–10 years.
• Types:
  • Calcium oxalate (about 80%, with calcium phosphate) — radio-opaque.
  • Uric acid (about 10%) — radiolucent on X-ray (but seen on CT); gout, high cell turnover (tumour lysis), acidic urine, diabetes, obesity.
  • Struvite (magnesium ammonium phosphate) — from urease-producing bacteria (e.g. Proteus); alkaline urine; staghorn calculi.
  • Cystine — cystinuria; young people; recurrent.
  • Drug stones — indinavir and others.
• Risk factors:
  • Dehydration; hot climates.
  • High salt and animal protein intake.
  • Obesity, diabetes, metabolic syndrome.
  • High urine calcium — idiopathic, primary hyperparathyroidism, sarcoidosis, excess vitamin D.
  • High urine oxalate — Crohn's disease or bowel resection (fat binds calcium in the gut, so more oxalate is absorbed), bariatric surgery, high vitamin C intake.
  • Low urine citrate — distal RTA, diarrhoea.
  • Gout; medullary sponge kidney; anatomical problems.
  • Drugs — topiramate, acetazolamide, calcium with vitamin D supplements in excess.

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Renal Colic

• Features:
  • Sudden, severe loin pain radiating to the groin (or testicle or labia), coming in waves.
  • The patient can't keep still (unlike peritonitis).
  • Nausea and vomiting.
  • Blood on dipstick in most (but not all).
  • Urinary frequency or urgency if the stone is near the bladder.
• Don't miss:
  • Ruptured abdominal aortic aneurysm — older person, "first renal colic" over 60, low BP; scan the aorta.
  • Ectopic pregnancy — pregnancy test in women of childbearing age.
  • Pyelonephritis or an infected obstructed kidney (fever).
  • Appendicitis, diverticulitis, biliary colic, testicular torsion.
• Tests:
  • Urine dipstick and culture; pregnancy test.
  • U&E, FBC, CRP; calcium and urate.
  • Low-dose non-contrast CT (CT KUB) within 24 hours (NICE NG118) — immediately if there is fever, a solitary kidney, or diagnostic doubt.
  • Ultrasound instead in pregnancy and in children.
• Pain relief (NICE):
  • NSAID first line by any route (e.g. diclofenac) — if not contraindicated (kidney impairment, bleeding, heart failure).
  • IV paracetamol if NSAIDs aren't suitable.
  • Opioids if both are unsuitable or not enough.
  • Don't use antispasmodics.
• Will it pass?
  • Most stones under 5 mm pass on their own (within about 4 weeks).
  • Alpha-blocker (tamsulosin) — consider for distal ureteric stones under 10 mm to help passage.
• Urgent decompression (nephrostomy or ureteric stent) if:
  • Infection with obstruction (fever, sepsis) — an emergency.
  • AKI, a solitary kidney, or both kidneys obstructed.
  • Uncontrolled pain or vomiting.
• Stone removal:
  • Shockwave lithotripsy (ESWL) — kidney stones under 2 cm, some ureteric stones.
  • Ureteroscopy (with laser) — ureteric stones and kidney stones under 2 cm.
  • Percutaneous nephrolithotomy (PCNL) — kidney stones over 2 cm and staghorn calculi.
  • NICE advises treating within 48 hours if pain persists and the stone is unlikely to pass.

⚠️ Safety Pearl: Fever with an obstructing stone is an infected obstructed kidney — antibiotics alone won't work. The kidney must be drained urgently (nephrostomy or stent).

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Preventing Stones

• For everyone:
  • Drink 2.5–3 L a day (aim for pale urine, over 2–2.5 L of urine a day); add lemon juice (citrate).
  • Reduce salt (raises urine calcium).
  • Keep normal calcium intake (700–1,200 mg/day) — don't cut down calcium; low dietary calcium increases oxalate absorption and stone risk.
  • Reduce animal protein; healthy weight.
  • Avoid fizzy drinks; limit high-oxalate foods if urine oxalate is high (spinach, rhubarb, nuts, chocolate, tea).
• Tests:
  • Stone analysis (sieve urine to catch it).
  • Serum calcium (exclude primary hyperparathyroidism), urate, U&E, bicarbonate.
  • 24-hour urine (calcium, oxalate, citrate, urate, volume) — for recurrent stone formers, children and high-risk patients.
• Drugs:
  • Potassium citrate — recurrent calcium stones with low urine citrate or high calcium; uric acid stones (alkalinises urine); distal RTA.
  • Thiazide diuretic — recurrent calcium stones with high urine calcium.
  • Allopurinol — uric acid stones or calcium stones with high urine urate.
  • Cystine stones — high fluid intake (over 3 L), urine alkalinisation, tiopronin.
  • Struvite stones — complete stone removal and treat infection.

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Lower Urinary Tract Infection

• Features: Dysuria, frequency, urgency, suprapubic pain, cloudy or smelly urine, visible haematuria.
• Organisms: E. coli (about 80%), Klebsiella, Proteus, Enterococcus, Staphylococcus saprophyticus (young women).
• Diagnosis (women under 65):
  • Based on symptoms — 2 or more of dysuria, new nocturia, cloudy urine suggests UTI.
  • Dipstick — nitrites (and leucocytes and blood) support it.
  • Don't dipstick people aged 65 or over or with catheters — bacteria are often present without infection; diagnose on symptoms and send a culture.
  • Exclude vaginal causes (discharge, itch) and STIs.
• Treatment — non-pregnant women (NICE NG109):
  • Consider a back-up prescription if symptoms are mild (many settle in 3–7 days).
  • First line:
    • Nitrofurantoin 100 mg modified-release twice daily for 3 days (if eGFR 45 or more).
    • Or trimethoprim 200 mg twice daily for 3 days (if low risk of resistance).
  • Second line: Pivmecillinam or fosfomycin (3 g single dose).
  • Simple analgesia; drink normally.
• Send a urine culture for: men, pregnancy, age 65 or over, catheters, recurrent UTI, treatment failure, visible haematuria, or risk of resistance.
• Recurrent UTI (NICE NG112 — 2 or more in 6 months or 3 or more in 12 months):
  • Look for a cause (ultrasound, post-void residual; stones; urology referral in men and with haematuria).
  • Advice — fluids, avoid holding urine, post-coital voiding.
  • Vaginal oestrogen after the menopause.
  • Methenamine hippurate (non-antibiotic option).
  • Antibiotic prophylaxis — single dose after sex, or daily low dose (nitrofurantoin or trimethoprim), reviewed every 6 months.

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UTI in Special Groups

• Men:
  • Always send a culture; treat for 7 days (nitrofurantoin or trimethoprim).
  • Consider prostatitis (perineal pain, fever, tender prostate) — longer courses (e.g. 14 days or more, quinolone or trimethoprim depending on sensitivity).
  • Refer to urology if recurrent, with haematuria, or with retention.
• Pregnancy:
  • Send a culture; treat for 7 days.
  • Nitrofurantoin (avoid at term — risk of neonatal haemolysis); amoxicillin or cefalexin depending on sensitivity.
  • Avoid trimethoprim in the first trimester (folate antagonist).
  • Asymptomatic bacteriuria is screened for and treated in pregnancy (risk of pyelonephritis and preterm birth).
  • Test of cure after treatment.
• Older people (65 or over):
  • Don't use dipsticks; don't treat asymptomatic bacteriuria.
  • New confusion alone is not enough to diagnose UTI — look for urinary symptoms, fever or rigors, and other causes of delirium.
• Catheter-associated UTI (NICE NG113):
  • Treat only if symptomatic (fever, loin pain, new confusion with no other cause) — all long-term catheters grow bacteria.
  • Change the catheter (if in place over 7 days) before starting antibiotics, and send a culture from the new catheter.
  • Treat for 7 days.
• Asymptomatic bacteriuria — don't treat, except in pregnancy and before urological procedures that breach the mucosa.

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Pyelonephritis

• Features:
  • Fever, rigors, loin pain and tenderness.
  • Nausea, vomiting.
  • Lower UTI symptoms may or may not be present.
  • Sepsis.
• Tests: Urine culture (always); blood cultures if unwell; U&E, FBC, CRP; pregnancy test.
• Admit if: signs of sepsis, unable to take oral fluids or drugs, pregnant, significant other illness, or not improving.
• Antibiotics (NICE NG111, non-pregnant adults; follow local policy):
  • Oral:
    • Cefalexin 500 mg twice or three times daily for 7–10 days.
    • Co-amoxiclav (only if culture shows it is sensitive).
    • Trimethoprim for 14 days (if sensitive).
    • Ciprofloxacin for 7 days — only if other antibiotics aren't suitable (MHRA warnings on fluoroquinolone side effects: tendon rupture, aortic aneurysm, neuropsychiatric).
  • IV (severe) — e.g. co-amoxiclav, cefuroxime, ceftriaxone, gentamicin (per local policy).
  • Pregnancy — cefalexin orally, or IV cefuroxime.
• Imaging (ultrasound or CT) if:
  • Not improving within 48–72 hours.
  • Suspected obstruction (stone) or abscess.
  • Men, recurrent pyelonephritis, or AKI.
• Complications:
  • Infected obstructed kidney — urgent drainage.
  • Renal or perinephric abscess — drainage and prolonged antibiotics.
  • Emphysematous pyelonephritis — gas in the kidney on CT, mainly in poorly controlled diabetes; life-threatening; drainage or nephrectomy.
  • Sepsis; AKI; papillary necrosis.
  • Xanthogranulomatous pyelonephritis — chronic, with staghorn stones; mimics cancer.

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Chronic Obstruction and Hydronephrosis

• Hydronephrosis — swelling of the kidney's collecting system from blocked urine flow. It can damage the kidney over weeks to months.
• Causes:
  • Bladder outlet — benign prostatic hyperplasia, prostate cancer, urethral stricture, neurogenic bladder (spinal cord injury, MS, diabetes).
  • Ureter — stones, pelvic tumours (cervix, bladder, rectum), lymph nodes, strictures (after surgery or radiotherapy).
  • Pelviureteric junction (PUJ) obstruction — often congenital; young people with loin pain after drinking large volumes (alcohol, caffeine).
  • Retroperitoneal fibrosis — fibrous tissue around the aorta traps the ureters (pulled towards the midline): back pain, AKI, high ESR; IgG4-related disease, aortic aneurysm, some drugs. Treat with steroids and stents.
  • Pregnancy (mild, physiological, more on the right).
• Features:
  • Often none (chronic obstruction is usually painless).
  • Loin ache; UTIs; stones.
  • Rising creatinine; hypertension.
  • Polyuria (tubular damage); hyperkalaemic acidosis (type 4 RTA).
  • Poor stream, dribbling, overflow incontinence (bladder outlet).
• Tests:
  • Ultrasound (kidneys, bladder, post-void residual).
  • CT (cause).
  • MAG3 renogram — shows whether the dilated system is really obstructed, and the share of function in each kidney.
• Treatment:
  • Relieve the obstruction — catheter, nephrostomy, ureteric stent, pyeloplasty (PUJ), prostate surgery.
  • Watch for post-obstructive diuresis.
  • Intermittent self-catheterisation for neurogenic bladder.

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The Kidney in Pregnancy

• Normal changes:
  • GFR rises by about 50% — so creatinine falls; a "normal" non-pregnant creatinine (e.g. over about 77 µmol/L) can be abnormal in pregnancy.
  • eGFR isn't valid in pregnancy.
  • Mild hydronephrosis, more on the right (hormones and pressure from the womb).
  • Glucose in the urine can be normal.
  • Sodium falls slightly; BP falls in the second trimester.
• Pre-eclampsia:
  • New hypertension after 20 weeks plus proteinuria (PCR 30 mg/mmol or more) or other organ damage (kidney, liver, platelets, brain, placenta).
  • Features — headache, visual disturbance, upper abdominal pain, oedema, brisk reflexes and clonus.
  • Prevention — aspirin 75–150 mg nightly from 12 weeks for women at high risk (CKD, previous pre-eclampsia, diabetes, lupus, chronic hypertension, antiphospholipid syndrome).
  • Treatment — labetalol (or nifedipine, methyldopa); magnesium sulfate to prevent seizures in severe disease; delivery is the cure.
  • Placental growth factor (PlGF) tests help diagnosis.
  • HELLP syndrome — haemolysis, raised liver enzymes, low platelets.
• AKI in pregnancy:
  • Early — hyperemesis gravidarum, miscarriage with sepsis.
  • Later — pre-eclampsia and HELLP, bleeding (placental abruption, postpartum haemorrhage), sepsis, acute fatty liver of pregnancy.
  • Thrombotic microangiopathy — TTP (often in pregnancy) and atypical HUS (often after delivery).
  • Obstruction (rare).
• Lupus flare or pre-eclampsia? — both cause proteinuria and hypertension; low complement, rising dsDNA and active urine sediment favour lupus; PlGF helps.
• Drugs: Avoid ACE inhibitors, ARBs, SGLT2 inhibitors and mycophenolate; take folic acid; check every drug.
• After pre-eclampsia — check BP, urine protein and creatinine at the 6–8 week postnatal review; long-term higher cardiovascular and kidney risk.

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Drug Reference Table