Does gouty nephropathy exist, and is it more common than we think?

Gout is present in one third of subjects with CKD but is usually an exclusion criterion in clinical trials investigating the role of uric acid in kidney disease. Bardin et al. report that one third of gouty subjects have hyperechoic medullas by ultrasound (consistent with crystalline deposits) that correlates with increased risk for hypertension and kidney dysfunction and which were not observed in >500 controls. If validated, a “gouty nephropathy” from microcrystalline deposits could be an important, unrecognized cause of CKD. Gout is present in one third of subjects with CKD but is usually an exclusion criterion in clinical trials investigating the role of uric acid in kidney disease. Bardin et al. report that one third of gouty subjects have hyperechoic medullas by ultrasound (consistent with crystalline deposits) that correlates with increased risk for hypertension and kidney dysfunction and which were not observed in >500 controls. If validated, a “gouty nephropathy” from microcrystalline deposits could be an important, unrecognized cause of CKD. A cross-sectional study of 502 patients found a diffuse hyperechoic kidney medulla pattern in patients with severe goutKidney InternationalVol. 99Issue 1PreviewWe have previously shown that ultrasonography can detect hyperechogenic crystal deposits in the kidney medulla of patients with gout. In this cross-sectional study we investigated the frequency and clinical correlates of hyperechogenic kidney medulla in 502 consecutive primary consultants for gout (ACR/EULAR criteria) at the Vien Gut medical center in Ho Chi Minh City, Vietnam. None of these patients received urate-lowering drugs. Kidney medulla echogenicity on B-mode ultrasonography was compared to that of the kidney cortex. Full-Text PDF Open AccessMedullary tophi: multiple microscopic lesions can amount to significant renal damageKidney InternationalVol. 99Issue 5PreviewWe read with great interest the study of Bardin et al., who found an association between long-standing untreated gout and medullary echogenicity, likely due to urate deposition.1 The linked commentary highlights the controversy regarding the pathogenetic role of gout in kidney damage and chronic kidney disease (CKD).2 The role of asymptomatic hyperuricemia remains unclear, but a recent study suggests that hyperuricemia with crystal deposition determines progression to CKD.3 A retrospective evaluation of 796 native kidney biopsies with abundant medulla identified tophi in only 4.5%, but this finding was strongly associated with CKD. Full-Text PDF