Chronic kidney disease — etiopathogenesis, diagnosis and management, with conservative management in the elderly

Definition and burden. CKD is a syndrome characterised by progressive and generally irreversible deterioration of renal function due to a reduction in nephron mass, present for more than three months with health implications. It is predominantly a disease of older adults — its incidence rises steadily with age and it is at least ten times more common at 75 years and above than between 15 and 45 years.

Causes in old age. The leading causes are hypertension and nephrosclerosis, diabetes mellitus, and obstructive uropathy. Two causes deserve special emphasis because they are potentially reversible: vascular disease of the main renal arteries and prostatic hypertrophy. In as many as one-third of older patients no specific cause can be identified. Also consider amyloidosis, myeloma and chronic interstitial nephritis from long-term NSAID use.

Etiopathogenesis — the mechanisms of progression. (a) Glomerular hyperfiltration in surviving nephrons — initially compensatory but ultimately accelerating glomerular sclerosis. (b) Retention of uraemic toxins — polyamines, guanidines, middle molecules and hormonal peptides. (c) A high parathyroid hormone level is itself a significant uraemic toxin. (d) Deficiency of erythropoietin and 1,25-dihydroxycholecalciferol → anaemia and hypocalcaemia. (e) Phosphate retention → secondary hyperparathyroidism and renal osteodystrophy. (f) Derangement of the renin–angiotensin–aldosterone system → hypertension, which in turn accelerates nephron loss.

Distinguish CKD from senile hypofiltration — a uniquely geriatric step. In older adults, senile hypofiltration differs from CKD because the glomerular filtration value is stable over 6–12 months, and there is no haematuria and no significant proteinuria (>0.30 g/day). Labelling every low eGFR in an 85-year-old as "CKD" causes unnecessary alarm, referral and treatment.

Clinical features. When creatinine clearance falls to about 25 mL/min the full picture of uraemia appears: a yellow-brown pallor, pruritus, asthenia, anorexia and vomiting; cardiovascular — hypertension, heart failure, pulmonary oedema, coronary disease, arrhythmias and pericarditis; neurological — polyneuropathy, clonus, asterixis and uraemic coma; endocrine — secondary hyperparathyroidism and hyperprolactinaemia; plus impaired cellular immunity and clotting abnormalities from platelet dysfunction.

Diagnosis and staging. Stage with eGFR (G1–G5) and albuminuria (A1–A3). Investigations: urinalysis and sediment, urine albumin–creatinine ratio, serum creatinine and electrolytes, bicarbonate, calcium, phosphate, intact PTH, haemoglobin and iron studies, and renal ultrasound for kidney size, symmetry and obstruction. Always exclude reversible contributors first — obstruction, volume depletion, infection, hypercalcaemia and nephrotoxic drugs.

Management — slowing progression. Blood pressure control, RAS blockade with a single agent for proteinuric disease (accept a creatinine rise of up to 30%; monitor potassium), glycaemic control individualised to frailty, statin therapy, smoking cessation, moderate protein intake with adequate calories to prevent sarcopenia, and avoidance of nephrotoxins — NSAIDs, aminoglycosides, iodinated contrast, and high-dose PPIs.

Management — treating the complications. Anaemia — iron repletion then an erythropoiesis-stimulating agent, targeting haemoglobin 10–11.5 g/dL, not normal. CKD–mineral and bone disorder — dietary phosphate restriction, phosphate binders, active vitamin D analogues, control of PTH. Metabolic acidosis — oral sodium bicarbonate to keep serum bicarbonate ≥22 mEq/L, which also protects muscle mass. Hyperkalaemia, volume overload, vaccination, and dose adjustment of every drug to the estimated GFR.

When to consider renal replacement. Textbook threshold: when GFR falls below 10 mL/min it becomes necessary to start replacement therapy — dialysis or transplantation. Age itself does not constitute a contraindication to either. In practice the decision is symptom-driven, and access should be planned well in advance (see Question 12).

Conservative kidney management (CKM) in the elderly — the second half of this question. CKM is an active, planned, non-dialytic pathway — not "no treatment". Its components are: (i) symptom control — pruritus, nausea, restless legs, breathlessness, fatigue and pain; (ii) medical management of anaemia, acidosis, fluid balance and blood pressure; (iii) dietary modification without inducing malnutrition; (iv) advance care planning and documentation of ceilings of care; (v) psychosocial, spiritual and carer support; and (vi) integration with palliative care. It is most appropriate where the predictors of poor dialysis outcome are present — poor nutritional status, dementia, gait disorders, impaired ADLs and IADLs, and late referral. The supporting figures: median survival on haemodialysis is 15.6 months at 80–84 years and 11.6 months at 85–89 years, and elective withdrawal accounts for 38% of deaths in the oldest dialysis patients — evidence that for the frail, dependent, multimorbid very old, dialysis may add little survival while costing function and time at home.

KDIGO 2024 CKD guideline — the shift from an eGFR-based to a risk-based approach. Key changes: stage CKD preferably with the race-free eGFRcr-cys equation (creatinine plus cystatin C) where cystatin C is available, and use eGFRcr-cys whenever creatinine-based eGFR is likely to be inaccurate; in CKD G3–G5, use an externally validated risk equation such as the Kidney Failure Risk Equation to estimate absolute risk of kidney failure and guide referral; SGLT2 inhibitors for adults with CKD regardless of diabetes — eGFR ≥20 with ACR ≥200 mg/g, or heart failure irrespective of albuminuria (Level 1A), and suggested for eGFR 20–45 with ACR <200 mg/g; non-steroidal MRA (finerenone) for type 2 diabetes with eGFR >25, normal potassium and persistent albuminuria on maximally tolerated RASi; statins for all adults over 50 with CKD G1–G5 not on dialysis; urate-lowering therapy only if symptomatic; and point-of-care creatinine and albumin testing where laboratory access is limited.

Indian context. India carries a heavy and partly distinct CKD burden, including CKD of unknown aetiology (CKDu) in agricultural belts of Andhra Pradesh, Odisha and Tamil Nadu, linked to heat stress, dehydration and agrochemical exposure. The Pradhan Mantri National Dialysis Programme under the National Health Mission provides free haemodialysis at district hospitals in public–private partnership mode, with an explicit policy push to expand peritoneal dialysis; AB-PMJAY and the Ayushman Vay Vandana Card (all citizens aged 70 and above) cover dialysis packages. Early detection depends on opportunistic screening for diabetes and hypertension through NPCDCS at health and wellness centres.