The Gouty Kidney: A Reappraisal

Author:

Bardin Thomas12,Letavernier Emmanuel34,Correas Jean-Michel5

Affiliation:

1. INSERM U1132 Unit, Hôpital Lariboisière, Université de Paris-Cité, 75010 Paris, France

2. French-Vietnamese Research Centre on Gout and Chronic Diseases, Vien Gut Medical Center, Ho Chi Minh City 70000, Vietnam

3. Service des Explorations Fonctionnelles Multidisciplinaires, Assistance Publique-Hôpitaux de Paris, Hôpital Tenon, 75020 Paris, France

4. Unité Mixte de Recherche (UMR) S 1155, Institut National de la Santé et de la Recherche Médicale, Hôpital Tenon, Sorbonne Université, 75020 Paris, France

5. Radiology Department, Hôpital Necker-Enfants Malades, Université Paris-Cité, 75015 Paris, France

Abstract

This review re-examines the role of crystal deposition in the kidney in view of recent clinical and experimental findings. The involvement of the renal system in gout seems frequent. Indeed, recent studies showed that approximately 25% of patients with gout experience renal failure, defined by estimated glomerular filtration rate <60 mL/min/1.73 m2. The pathophysiology is complex and involves several factors, their respective roles being difficult to dissect. The role of crystal deposition in the kidney was the first suspected, and the concept of gouty microcrystalline nephropathy, also called gouty nephropathy, has been popular, supported by early autopsy studies demonstrating uric acid and urate crystal deposition in the renal medulla of patients with gout, together with features of tubulointerstitial nephritis. Crystal deposition was first considered an important source of renal involvement in gout. After the introduction of urate-lowering drugs and the performance of kidney biopsies, which mainly involved the renal cortex and did not reveal much crystal deposition but rather vascular changes, this concept has been criticized and even dismissed. Thereafter, kidney involvement in gout was considered mainly vascular, related to hypertension and associated comorbidities and later to hyperuricemia. The toxic effects of non-steroidal anti-inflammatory drugs is also an important factor. Modern imaging, especially renal ultrasonography, allows for atraumatic exploration of the kidney and has revealed hyperechogenicity of the renal medulla, suggesting crystalline deposits, in approximately one-third of patients with tophaceous gout. Experimental models of gouty nephropathy have recently demonstrated the pathogenic role of microcrystal deposition in the collecting ducts and parenchyma of the renal medulla. Taken together, these recent findings lead to the re-examination of the pathogenic role of crystal deposition in the renal medulla and testing the effect of urate-lowering drugs on renal features of gouty patients with evidence of renal crystal deposition.

Publisher

MDPI AG

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