Clinical co-management of gouty nephropathy: A bidirectional interface between rheumatology and nephrology

Gouty nephropathy is a complex clinical condition that intertwines rheumatology and nephrology, characterized by a bidirectional pathophysiological relationship in which hyperuricemia leads to kidney damage while chronic kidney disease (CKD) exacerbates urate deposition. This intricate interplay presents unique diagnostic and therapeutic challenges that necessitate coordinated management. A comprehensive literature analysis spanning from 1970 to 2025 was conducted using PubMed and Cochrane databases, along with clinical guidelines, to synthesize evidence regarding gout pathophysiology, renal urate handling, manifestations of acute and chronic nephropathy, and management strategies in CKD. Key findings indicate that uric acid (UA) solubility is pH-dependent, with significant implications for crystal nephropathy pathogenesis. Renal handling of UA involves glomerular filtration followed by proximal tubule reabsorption, with only a small percentage ultimately excreted. In CKD, impaired urate excretion leads to disproportionate hyperuricemia. The dialysis paradox is evident, as hemodialysis (HD) can rapidly lower serum urate (SUA) levels but may trigger flares in a notable percentage of patients due to crystal mobilization. Diagnostic challenges arise because acute gout flares can present with normal UA levels during inflammation, complicating biomarker interpretation in CKD. Dual-energy CT (DECT) has demonstrated high specificity for crystal detection but reduced sensitivity in early gout. Management in advanced CKD requires careful consideration of renal dosing for xanthine oxidase inhibitors (XOIs), flare prophylaxis with low-dose colchicine or prednisone, and the use of SGLT2 inhibitors for uricosuria in diabetic patients, while avoiding NSAIDs and thiazides. Interdisciplinary coordination is crucial, requiring nephrology referrals for unexplained renal decline or stones, rheumatology referrals for refractory gout or tophi, and shared decision-making for urate-lowering therapy (ULT) selection. Effective management of gouty nephropathy ultimately depends on integrating expertise from both fields, implementing evidence-based medication adjustments for renal impairment, and establishing standardized co-management protocols to address ongoing research gaps in advanced CKD populations.

Authors

Publication Details

Journal
Batna Journal of Medical Sciences (BJMS)
Published
2025-08-25
DOI
https://doi.org/10.48087/bjmsra.2025.12326
Primary Topic
Gout, Hyperuricemia, Uric Acid
Type
article
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article

Clinical co-management of gouty nephropathy: A bidirectional interface between rheumatology and nephrology

Fareed Omar, Kamel Remita, Wafa FEDHILA
Batna Journal of Medical Sciences (BJMS)
Gout, Hyperuricemia, Uric Acid
article

Clinical co-management of gouty nephropathy: A bidirectional interface between rheumatology and nephrology

Fareed Omar, Kamel Remita, Wafa FEDHILA
article en

Abstract

Gouty nephropathy is a complex clinical condition that intertwines rheumatology and nephrology, characterized by a bidirectional pathophysiological relationship in which hyperuricemia leads to kidney damage while chronic kidney disease (CKD) exacerbates urate deposition. This intricate interplay presents unique diagnostic and therapeutic challenges that necessitate coordinated management. A comprehensive literature analysis spanning from 1970 to 2025 was conducted using PubMed and Cochrane databases, along with clinical guidelines, to synthesize evidence regarding gout pathophysiology, renal urate handling, manifestations of acute and chronic nephropathy, and management strategies in CKD. Key findings indicate that uric acid (UA) solubility is pH-dependent, with significant implications for crystal nephropathy pathogenesis. Renal handling of UA involves glomerular filtration followed by proximal tubule reabsorption, with only a small percentage ultimately excreted. In CKD, impaired urate excretion leads to disproportionate hyperuricemia. The dialysis paradox is evident, as hemodialysis (HD) can rapidly lower serum urate (SUA) levels but may trigger flares in a notable percentage of patients due to crystal mobilization. Diagnostic challenges arise because acute gout flares can present with normal UA levels during inflammation, complicating biomarker interpretation in CKD. Dual-energy CT (DECT) has demonstrated high specificity for crystal detection but reduced sensitivity in early gout. Management in advanced CKD requires careful consideration of renal dosing for xanthine oxidase inhibitors (XOIs), flare prophylaxis with low-dose colchicine or prednisone, and the use of SGLT2 inhibitors for uricosuria in diabetic patients, while avoiding NSAIDs and thiazides. Interdisciplinary coordination is crucial, requiring nephrology referrals for unexplained renal decline or stones, rheumatology referrals for refractory gout or tophi, and shared decision-making for urate-lowering therapy (ULT) selection. Effective management of gouty nephropathy ultimately depends on integrating expertise from both fields, implementing evidence-based medication adjustments for renal impairment, and establishing standardized co-management protocols to address ongoing research gaps in advanced CKD populations.

Batna Journal of Medical Sciences (BJMS)Vol. 12(3)
Openalex Percentile: Top 74%
Gout, Hyperuricemia, Uric Acid
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