Laboratory tests - urea, electrolyte, and creatinine

Two purposes

U&E/creatinine monitoring in rheumatology serves two distinct purposes: detecting renal involvement by the rheumatic disease itself (particularly lupus nephritis, vasculitis) and monitoring for nephrotoxicity from rheumatological drug therapy
Routine, regular monitoring is standard practice for most patients on disease-modifying antirheumatic drugs and for any patient with a condition carrying renal involvement risk (SLE, vasculitis)

Renal involvement in SLE (lupus nephritis) and ANCA-associated vasculitis reflects direct immune-mediated glomerular injury - a rising creatinine and/or new proteinuria/haematuria in these conditions should prompt urgent reassessment and consideration of renal biopsy, not simply be attributed to age/dehydration without specific exclusion of active renal disease
NSAIDs (reduced renal perfusion via prostaglandin inhibition, particularly risky with concurrent ACEi/ARB/diuretic - the "triple whammy"), methotrexate (renally cleared - reduced clearance risks accumulation and toxicity, and methotrexate itself can be nephrotoxic at high doses), and ciclosporin (direct nephrotoxicity) are among the rheumatological drugs requiring specific renal monitoring

A rising creatinine in a patient with known SLE or vasculitis should prompt urgent workup for active renal involvement (urinalysis, urine protein:creatinine ratio, renal biopsy consideration) given the time-critical nature of treating active lupus nephritis or renal vasculitis before irreversible damage accrues
Baseline and regular renal function monitoring is required before and during treatment with several DMARDs, with dose adjustment or cessation for significant decline

Deteriorating renal function generally requires distinguishing disease-driven (escalate immunosuppression) from drug-induced (reduce/stop the causative drug) causes - as with cytopenias, the correct response differs by cause, and the two can occasionally coexist
NSAID dose/duration should be minimised in patients with any renal risk factors, given the "triple whammy" interaction risk specifically

Lupus nephritis, ANCA-associated vasculitis with renal involvement, methotrexate/NSAID/ciclosporin nephrotoxicity, the "triple whammy" (NSAID + ACEi/ARB + diuretic)

Renal function decline in a rheumatic disease patient is never assumed benign by default - the differential (active disease vs drug toxicity vs an unrelated cause) must be actively worked through given how different, and how time-critical, the correct response can be for each

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