Log in / Register Soon
Official Education Partner of the Delhi Medicos Premier League — free question bank for every player and college
SN6 SHORT NOTE 5M

Write a short note on the clinical assessment of kidney disease.

General Medicine · Final Professional

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 CHRONICFavouring ACUTE
Previous abnormal creatinine (the most reliable evidence)Documented normal recent creatinine
Small, echogenic kidneys with loss of corticomedullary differentiationNormal-sized kidneys
Anaemia (erythropoietin deficiency)Normal haemoglobin
Hypocalcaemia with hyperphosphataemia and raised PTH (established bone disease)Normal calcium/phosphate metabolism
Broad waxy castsMuddy brown or red cell casts
Long-standing symptoms; nocturia; pruritus; peripheral neuropathyAbrupt 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":
FindingSignificance
RED CELL CASTS, dysmorphic red cellsGLOMERULONEPHRITIS — diagnostic of glomerular bleeding
Muddy brown granular castsAcute tubular necrosis
White cell castsPyelonephritis, interstitial nephritis
Oval fat bodies, "Maltese crosses"Nephrotic syndrome
Broad waxy castsChronic kidney disease
EosinophiluriaAcute interstitial nephritis (insensitive)
CrystalsStones, 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.
CLINICAL PEARL

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

  1. Q1Discuss the aetiology, clinical features, complications, investigations and management of chronic kidney disease. ★
  2. Q2Discuss the causes, clinical features, investigations and management of acute kidney injury, including acute tubular necrosis. ★
  3. Q3Discuss the aetiology, pathophysiology, clinical features, complications and management of nephrotic syndrome. ★
  4. SN1Write a short note on nephritic syndrome and acute glomerulonephritis, including post-streptococcal glomerulonephritis.
  5. SN2Write a short note on rapidly progressive glomerulonephritis.
  6. SN3Write a short note on proteinuria and microalbuminuria.
  7. SN4Write a short note on urinary tract infection and acute pyelonephritis.
  8. SN5Write a short note on renal replacement therapy — haemodialysis, peritoneal dialysis and transplantation.
  9. SN6Write a short note on the clinical assessment of kidney disease.
  10. SN7Write a short note on renal artery stenosis.
  11. SN8Write a short note on autosomal dominant polycystic kidney disease.

Every General Medicine chapter →

Scroll to Top