Pharmacology of major drug classes used to treat kidney disease

Drug classes

Drug classes central to nephrology practice span RAAS blockade (renoprotection), diuretics (volume management), and renal-specific agents (phosphate binders, ESAs, immunosuppression) - plus the universal need to adjust dosing for reduced renal clearance

Class	Renal role
ACEi/ARB	Reduce intraglomerular pressure (efferent arteriolar dilation) - renoprotective in proteinuric CKD/diabetic nephropathy, independent of BP lowering
SGLT2 inhibitors	Reduce intraglomerular pressure via tubuloglomerular feedback - now a cornerstone renoprotective therapy across CKD aetiologies, not just diabetes
Loop diuretics	Volume management - efficacy preserved even in advanced CKD (unlike thiazides)
Phosphate binders	Reduce GI phosphate absorption - CKD-MBD management
Erythropoiesis-stimulating agents (ESAs)	Replace deficient endogenous EPO - anaemia of CKD
Immunosuppressants	Glomerulonephritis treatment, transplant maintenance

Renally-cleared drugs accumulate in CKD, making dose adjustment (or avoidance) one of the most common medication safety issues in nephrology practice

Dose-adjust or avoid renally-cleared drugs as eGFR falls (e.g. reduce or avoid metformin, many antibiotics, DOACs at very low eGFR)
SGLT2 inhibitors - renoprotective benefit demonstrated across diabetic and non-diabetic proteinuric CKD (DAPA-CKD, EMPA-KIDNEY); generally continued down to low eGFR thresholds per current guidance, then reassessed
ACEi/ARB - expect and tolerate an initial eGFR dip (up to ~30%) after starting; stop only if the rise is progressive or accompanied by hyperkalaemia, not for an isolated acceptable initial dip

CKD-MBD, anaemia of CKD, diabetic nephropathy, glomerulonephritis, drug-induced nephrotoxicity

The evidence base for renoprotective drug classes (RAAS blockade, then SGLT2 inhibitors) has progressively broadened CKD treatment from purely supportive to genuinely disease-modifying

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