Chronic Kidney Disease
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Direct answer
Abnormalities of kidney structure or function persisting beyond three months define chronic kidney disease, staged G1 to G5 by eGFR alongside albuminuria categories A1 to A3. The commonest cause in India is diabetic kidney disease, followed by hypertension and chronic glomerulonephritis. The pillars of therapy are renin-angiotensin blockade with an ACE inhibitor or ARB in albuminuric disease, SGLT2 inhibitors which protect the kidney with or without diabetes, blood pressure and glycaemic control, and avoidance of nephrotoxins; dialysis is reserved for uraemic or refractory complications, while transplantation offers the best long-term outcome.
What you must remember
- Staging by eGFR (mL/min/1.73 m2): G1 90 or above with damage markers, G2 60 to 89, G3a 45 to 59, G3b 30 to 44, G4 15 to 29, G5 below 15 (kidney failure); albuminuria A1 below 30, A2 30 to 300, A3 above 300 mg per gram creatinine.
- Complications: normocytic anaemia from erythropoietin deficiency (iron and erythropoiesis-stimulating agents), mineral bone disease with high phosphate, low calcium and high PTH, metabolic acidosis, hyperkalaemia and accelerated atherosclerosis.
- Renoprotection: ACE inhibitor or ARB for albuminuria, SGLT2 inhibitors (dapagliflozin, empagliflozin) even in non-diabetic CKD, finerenone in diabetic kidney disease, blood pressure and HbA1c control, smoking cessation.
- Avoid NSAIDs and nephrotoxic drugs, adjust doses to eGFR, restrict salt and treat acidosis with sodium bicarbonate.
- Dialysis indications: refractory hyperkalaemia or acidosis, fluid overload with pulmonary oedema, uraemic pericarditis, encephalopathy or bleeding — pericarditis is an absolute urgency; plan replacement as a symptomatic stage 5 patient approaches eGFR around 5 to 10.
- Ultrasound shows small echogenic kidneys (normal or large in diabetic nephropathy, obstruction, amyloidosis, polycystic disease).
- Renal osteodystrophy spans osteitis fibrosa cystica from high PTH, adynamic bone disease and osteomalacia; treated with phosphate binders, active vitamin D analogues and parathyroidectomy for refractory disease.
Planning care for a newly detected creatinine of 3.4
A 56-year-old diabetic, hypertensive man has creatinine 3.4 mg per dL; is this acute or chronic? Duration decides, and the evidence assembles: normocytic anaemia, raised PTH with low calcium and high phosphate, and small echogenic kidneys on ultrasound. (Keep large kidneys for diabetic nephropathy, obstruction, amyloidosis, polycystic disease.) Convert creatinine to eGFR — 22 with albumin-to-creatinine ratio 900, so G4 A3 — because a normal-looking creatinine in the elderly or malnourished masks a low filtration rate, and staging drives everything downstream. The renoprotective prescription: an ACE inhibitor or ARB for the albuminuria, an SGLT2 inhibitor protecting the kidney with or without diabetes, finerenone in diabetic kidney disease, blood pressure and HbA1c control, smoking cessation, salt restriction, sodium bicarbonate for acidosis, and an explicit ban on NSAIDs with dose adjustment of everything else. Manage the complications on a schedule: iron and erythropoiesis-stimulating agents for the anaemia; vigilance for hyperkalaemia and accelerated atherosclerosis. Plan the endpoint deliberately: a symptomatic stage 5 patient approaches replacement as eGFR nears 5 to 10, ideally with a pre-emptive transplant work-up; the urgent indications — refractory hyperkalaemia or acidosis, pulmonary oedema, uraemic pericarditis, encephalopathy — override planning.
Where students slip
Acute versus chronic is decided by duration, kidney size, anaemia, bone disease and any prior creatinine — and the exam hides the duration in the history while displaying the creatinine, so the small echogenic kidney on the ultrasound line is the tell. The "normal creatinine" in the sarcopenic elderly is the second trap; always convert to eGFR, and stage with the albuminuria category beside it. The drug-evidence set is the third: ACE inhibitor or ARB for albuminuria, SGLT2 inhibitors even without diabetes, finerenone in diabetic disease — older lists without the latter two are the distractor options. And dialysis is initiated for failure of medical management or uraemic emergencies, not for a laboratory number alone; the vignette of a stable G5 patient without indications asks for preparation, not a catheter.
Frequently asked questions
How is CKD defined and staged?
Structural or functional kidney abnormalities for over three months, staged G1 to G5 by eGFR and A1 to A3 by albuminuria; both predict progression and outcomes.
Why does anaemia develop in CKD?
Falling erythropoietin production plus uraemic inhibition of erythropoiesis cause normocytic normochromic anaemia; treated with iron and erythropoiesis-stimulating agents.
Which drugs slow CKD progression?
ACE inhibitors or ARBs in albuminuric disease, SGLT2 inhibitors with or without diabetes, and finerenone in diabetic kidney disease.
Which CKD causes keep the kidneys large?
Diabetic nephropathy, polycystic kidney disease, obstructive uropathy, amyloidosis and multiple myeloma; most other chronic diseases shrink the kidneys.
List the urgent indications for dialysis.
Refractory hyperkalaemia, severe acidosis, fluid overload with pulmonary oedema, and uraemic emergencies — pericarditis, encephalopathy and bleeding.
What is renal osteodystrophy?
Bone disease in CKD — osteitis fibrosa from secondary hyperparathyroidism, adynamic bone and osteomalacia — managed with phosphate binders, vitamin D analogues and sometimes parathyroidectomy.