Write a short note on the clinical assessment of kidney disease.
The Four Questions
A structured approach to any patient with suspected renal disease answers four questions in order:
1. Is the disease ACUTE or CHRONIC?
2. Where is the lesion — pre-renal, glomerular, tubulointerstitial, vascular or post-renal?
3. How severe is it — and are there immediate threats to life?
4. What is the underlying cause?
Acute or Chronic?
| Favouring CHRONIC | Favouring ACUTE |
|---|---|
| Previous abnormal creatinine (the most reliable evidence) | Documented normal recent creatinine |
| Small, echogenic kidneys with loss of corticomedullary differentiation | Normal-sized kidneys |
| Anaemia (erythropoietin deficiency) | Normal haemoglobin |
| Hypocalcaemia with hyperphosphataemia and raised PTH (established bone disease) | Normal calcium/phosphate metabolism |
| Broad waxy casts | Muddy brown or red cell casts |
| Long-standing symptoms; nocturia; pruritus; peripheral neuropathy | Abrupt onset |
Remember two exceptions: kidneys are normal or enlarged in chronic disease due to diabetic nephropathy, amyloidosis, polycystic disease, myeloma or HIV nephropathy; and acute-on-chronic disease is common — a patient may have both.
History
- Urinary symptoms: oliguria, anuria, polyuria, nocturia (an early sign of impaired concentrating ability), frequency, dysuria, hesitancy and poor stream (obstruction), frothy urine (proteinuria), haematuria and its timing and colour.
- Systemic symptoms: oedema, breathlessness, fatigue, anorexia, nausea, pruritus, weight loss, fever, rash, arthralgia, haemoptysis.
- Past history: diabetes and its duration, hypertension, recurrent UTI or childhood enuresis, stones, prostatic symptoms, gout, recent infection (sore throat, skin sepsis, diarrhoea), pregnancy complications, autoimmune disease.
- DRUG HISTORY — critical: NSAIDs and analgesics (including long-term over-the-counter use), ACE inhibitors and ARBs, aminoglycosides, contrast exposure, chemotherapy, proton pump inhibitors, lithium, and traditional, ayurvedic and herbal preparations, which may contain heavy metals or aristolochic acid and are a genuine and under-recognised cause of interstitial nephritis in India.
- Family history: polycystic kidney disease, Alport syndrome (with deafness), hereditary nephritis, and consanguinity.
- Occupational and environmental: heavy metal exposure, agrochemicals, heat stress (relevant to CKD of unknown aetiology in agricultural communities).
Examination
- General: anaemia, uraemic sallow pigmentation, scratch marks, bruising, uraemic fetor, oedema (periorbital and dependent), nutritional status.
- BLOOD PRESSURE — in every patient, both a cause and a consequence of renal disease; postural measurement to assess volume status.
- Volume status — JVP, skin turgor, mucous membranes, capillary refill, lung bases, sacral and pedal oedema, daily weight.
- Abdomen: ballotable kidneys (polycystic disease, hydronephrosis, tumour), palpable bladder (obstruction — never omit this), renal bruit (renal artery stenosis), hepatomegaly.
- Rectal examination for prostatic enlargement in men with obstructive symptoms.
- Fundoscopy — diabetic or hypertensive retinopathy; retinopathy strongly supports diabetic nephropathy as the cause of proteinuria.
- Systemic clues: rash (vasculitis, SLE), joints, nasal crusting and saddle nose (GPA), hearing (Alport), neuropathy, pericardial rub (uraemic pericarditis — an indication for dialysis), asterixis.
Investigations
Urine — the most informative and most neglected investigation:
- Dipstick: protein, blood, leucocytes, nitrites, glucose, pH.
- MICROSCOPY OF FRESH URINE — "the renal biopsy of the poor":
| Finding | Significance |
|---|---|
| RED CELL CASTS, dysmorphic red cells | GLOMERULONEPHRITIS — diagnostic of glomerular bleeding |
| Muddy brown granular casts | Acute tubular necrosis |
| White cell casts | Pyelonephritis, interstitial nephritis |
| Oval fat bodies, "Maltese crosses" | Nephrotic syndrome |
| Broad waxy casts | Chronic kidney disease |
| Eosinophiluria | Acute interstitial nephritis (insensitive) |
| Crystals | Stones, drug crystals, oxalate (ethylene glycol) |
- Quantify protein: urine protein:creatinine or albumin:creatinine ratio.
- Culture where infection is suspected; three early-morning samples for AFB and CBNAAT in sterile pyuria.
Blood:
- Creatinine with eGFR, urea, electrolytes, bicarbonate; cystatin C where muscle mass is atypical.
- CBC (anaemia), calcium, phosphate, PTH, alkaline phosphatase, vitamin D, uric acid, albumin, glucose and HbA1c, lipids.
- Immunological panel where indicated: ANA, anti-dsDNA, complement C3/C4, ANCA, anti-GBM, immunoglobulins, cryoglobulins, hepatitis B and C, HIV, ASO.
- Serum and urine protein electrophoresis with immunofixation and serum free light chains — essential in anyone over 50 with unexplained renal impairment, since myeloma is a classic missed diagnosis.
Imaging:
- ULTRASOUND KIDNEYS AND BLADDER — the essential first imaging test in every patient: kidney size, echogenicity, corticomedullary differentiation, hydronephrosis (obstruction), cysts, stones, and post-void residual volume.
- Doppler for renal artery stenosis and renal vein thrombosis.
- CT (non-contrast for stones); avoid contrast where possible, and hydrate if unavoidable. Avoid gadolinium in advanced CKD because of nephrogenic systemic fibrosis.
- Radionuclide scans for differential function and obstruction; MCUG and DMSA in children.
Renal Biopsy:
- Indications: unexplained AKI, nephrotic syndrome in adults, glomerulonephritis, systemic disease with renal involvement, unexplained proteinuria or haematuria with impaired function, and transplant dysfunction.
- Contraindications: bleeding diathesis or uncorrected coagulopathy, uncontrolled hypertension, single kidney (relative), small shrunken kidneys, active infection, and an uncooperative patient.
- Complications: haematuria, perinephric haematoma, arteriovenous fistula, and rarely nephrectomy or death — so it must be justified by a clear question that will change management.
Look at the urine yourself. A fresh, spun urine sample examined under the microscope will distinguish glomerulonephritis from acute tubular necrosis from interstitial nephritis in minutes, at almost no cost — and it is the one investigation most often outsourced, delayed or skipped. Red cell casts mean glomerulonephritis and demand urgent serology and biopsy; muddy brown casts mean ATN and demand attention to perfusion and nephrotoxins. Those two findings, obtained at the bedside, redirect the whole management.
All questions in Nephrology
- Q1Discuss the aetiology, clinical features, complications, investigations and management of chronic kidney disease. ★
- Q2Discuss the causes, clinical features, investigations and management of acute kidney injury, including acute tubular necrosis. ★
- Q3Discuss the aetiology, pathophysiology, clinical features, complications and management of nephrotic syndrome. ★
- SN1Write a short note on nephritic syndrome and acute glomerulonephritis, including post-streptococcal glomerulonephritis.
- SN2Write a short note on rapidly progressive glomerulonephritis.
- SN3Write a short note on proteinuria and microalbuminuria.
- SN4Write a short note on urinary tract infection and acute pyelonephritis.
- SN5Write a short note on renal replacement therapy — haemodialysis, peritoneal dialysis and transplantation.
- SN6Write a short note on the clinical assessment of kidney disease.
- SN7Write a short note on renal artery stenosis.
- SN8Write a short note on autosomal dominant polycystic kidney disease.