Chronic Kidney Disease and Complications — Advanced

G categories are based on eGFR: G3a is 45–59, G3b is 30–44, G4 is 15–29, G5 is <15 mL/min/1.73 m2. The patient's eGFR of 42 places him in G3b. Albuminuria categories (using common UK units) are A1 <3 mg/mmol, A2 3–30 mg/mmol, A3 >30 mg/mmol. His uACR of 35 mg/mmol is A3. Therefore the correct KDIGO descriptor is G3b A3. Other options are incorrect because they misclassify either the G or A category.

When hyperkalaemia produces ECG changes (peaked T waves, QRS widening), the immediate priority is to stabilise the cardiac membrane with intravenous calcium (usually calcium gluconate or calcium chloride). This does not reduce serum potassium but reduces arrhythmic risk. Measures to lower potassium (insulin with glucose, nebulised salbutamol, bicarbonate if acidotic, or dialysis) follow or are given concurrently as appropriate. Enteral sodium polystyrene sulfonate and oral patiromer act slowly and are not suitable for immediate stabilisation. Haemodialysis is definitive in refractory or severe cases but is not the first immediate action to protect the myocardium.

Chronic metabolic acidosis in CKD (serum bicarbonate persistently <22 mmol/L) is commonly treated with oral sodium bicarbonate to correct acidosis, improve nutrition and slow progression of muscle wasting. Acetazolamide causes bicarbonate wasting and would worsen metabolic acidosis. Urgent haemodialysis is not indicated solely for mild–moderate chronic metabolic acidosis unless there are other indications for dialysis. Dietary measures alone are insufficient to correct serum bicarbonate.

In CKD-related anaemia, iron deficiency should be corrected before starting erythropoiesis-stimulating agents (ESAs). Ferritin 40 µg/L and transferrin saturation 12% indicate iron deficiency. In non-dialysis CKD, a trial of oral iron is generally appropriate as the initial step unless there is intolerance, poor absorption, or need for rapid repletion—then intravenous iron is used. ESAs are generally considered after iron repletion if Hb remains low (typically when Hb persistently <10 g/dL and other causes excluded). Bone marrow biopsy is not first-line for suspected iron-deficiency anaemia in CKD, and transfusion is reserved for symptomatic anaemia or acute needs.

When PTH is elevated and 25-hydroxyvitamin D is low in CKD, the initial step is to correct vitamin D deficiency with nutritional vitamin D such as cholecalciferol or ergocalciferol. Calcium-containing phosphate binders are used for selected hyperphosphataemia, not isolated PTH elevation with normal phosphate. Oral cinacalcet and parathyroidectomy are generally reserved for severe or refractory secondary hyperparathyroidism after appropriate medical management; cinacalcet is not an intravenous drug. Diet alone will not correct vitamin D deficiency.

Guideline recommendations support offering a statin (with or without ezetimibe) for adults with CKD not on dialysis who are of typical age for primary prevention (KDIGO suggests most adults ≥50 years). Statins reduce atherosclerotic events in non-dialysis CKD. Starting dialysis alters indications and does not necessarily mean starting a statin de novo. Statins are not contraindicated in CKD stage 4. Aspirin is not an alternative to statins for primary prevention in this context and decisions should be individualised. LDL thresholds alone are not the sole determinant for statin use in CKD as guidelines recommend considering CKD itself as a risk marker.

NICE and other guidance advise that metformin can be continued with caution when eGFR is 30–45 mL/min/1.73 m2 with dose reduction and close monitoring; it should be stopped when eGFR is <30 or if there is intercurrent illness with AKI risk. Therefore the appropriate action is to reduce the dose and monitor renal function regularly. Permanently stopping metformin is unnecessary at this eGFR. Switching agents or giving IV fluids are not the standard immediate actions; IV fluids are only relevant if there is volume depletion/AKI.

For patients likely to start haemodialysis within months, timely referral for creation of a native arteriovenous fistula (AVF) is recommended because AVFs have superior long-term outcomes compared with central venous catheters. Delaying referral risks starting dialysis with a catheter. Choice of modality (haemodialysis versus peritoneal dialysis) is individualised, but planning for AVF when haemodialysis is anticipated is appropriate. ESAs do not meaningfully delay the need for dialysis in this context. A central venous catheter is not preferred as long-term access due to higher complication rates.

Uraemic pericarditis/pericardial effusion in patients with inadequate dialysis is best managed by intensifying or urgently resuming dialysis to remove uraemic toxins; this often leads to resolution. NSAIDs are generally avoided because of nephrotoxicity and bleeding risk. Pericardiocentesis is reserved for cardiac tamponade or large symptomatic effusions not responsive to dialysis. Corticosteroids are not standard therapy for uraemic pericarditis. Observation alone is inappropriate in a symptomatic patient with missed dialysis sessions.

Newer potassium binders such as patiromer and sodium zirconium cyclosilicate can effectively control chronic hyperkalaemia and are used to enable continued RAAS inhibitor therapy in patients who benefit from these drugs. Permanently stopping RAAS blockade forfeits proven renal/cardiovascular benefits. Dietary measures may help but are often insufficient alone. Old exchange resins (sodium polystyrene sulfonate) have limited evidence for long-term use and safety concerns; they are not the preferred long-term strategy. Switching to another agent with similar RAAS effects is unlikely to avoid hyperkalaemia; there are no direct alternatives that preserve the same benefits without hyperkalaemia risk.