Progression of Minimal-Change Glomerulopathy to Focal Glomerulosclerosis in a Patient with Fenoprofen Nephropathy

Artinano, Mauricio; Etheridge, Whitson B.; Stroehlein, Kristina B.; Barcenas, Camilo G.

doi:10.1159/000167189

Cited by 15 publications

(8 citation statements)

References 7 publications

(9 reference statements)

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“…However, the injury seen on LM and electron microscopy (EM) examination is a tubular one rather than glomerular [31][32][33][34][35][36][37][38][39][40]. In our neonatal rat model, under the same regimen as in the study described here, significant glomerular injury was noted on EM examination [13].…”

Section: Discussionmentioning

confidence: 96%

Indomethacin, ibuprofen and gentamicin administered during late stages of glomerulogenesis do not reduce glomerular number at 14 days of age in the neonatal rat

et al. 2009

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Premature neonates are frequently administered indomethacin, ibuprofen and gentamicin during the period of active glomerulogenesis. These drugs are known to have nephrotoxic effects, but the morphological effect of these drugs is unknown. The purpose of this study was to determine whether administration of these drugs during the late stages of glomerulogenesis in the rat has an effect on glomerular endowment. Rat pups were given, intraperitoneally, indomethacin, ibuprofen or indomethacin and gentamicin for the first 5 days of their postnatal life. The pups were killed at 14 days of age at completion of glomerulogenesis. The total number of glomeruli in the left kidney was determined by the physical disector/fractionator stereological technique. There was no difference between treatment groups in total number of glomeruli per kidney (P = 0.45). There were significantly fewer glomeruli per gram of kidney in those rat pups that had received indomethacin or ibuprofen (P < 0.0001). The reduction in the number of glomeruli per gram of kidney may indicate augmented growth of nephron tubules and/or collecting ducts, and/or be a consequence of oedema secondary to drug exposure. Further study is required to determine whether reduced glomerular number is seen in older animals or following exposure to these drugs at different time-points in kidney development.

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Section: Discussionmentioning

confidence: 96%

Indomethacin, ibuprofen and gentamicin administered during late stages of glomerulogenesis do not reduce glomerular number at 14 days of age in the neonatal rat

et al. 2009

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“…There have been a number of case reports of focal glomerulosclerosis, membranous glomer- ulonephritis, or proliferative glomerulonephritis associated with NSAID treatment in adult humans. However, because of their rarity it is difficult to determine whether this is causative or incidental (31)(32)(33)(34). Gentamicin causes acute tubular necrosis that may also be associated with tubulointerstitial changes seen on LM (35)(36)(37).…”

Section: Discussionmentioning

confidence: 99%

Renal Glomeruli and Tubular Injury Following Indomethacin, Ibuprofen, and Gentamicin Exposure in a Neonatal Rat Model

et al. 2007

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Indomethacin, ibuprofen, and gentamicin are commonly administered to neonates between 24 and 28 wk gestation when glomerulogenesis is still occurring. Indomethacin is known to cause renal failure in up to 25% of infants treated. Possible morphologic effects of these drugs are largely unknown. The purpose of this study was to determine the type of renal changes found on light (LM) and electron microscopy (EM) following administration of indomethacin, ibuprofen, and gentamicin in a neonatal rat model. Rat pups were exposed to indomethacin or ibuprofen and/or gentamicin antenatally for 5 d before birth or postnatally for 5 d from d 1 of life. Pups were killed at 14 d of age. LM examination in all indomethacin-and ibuprofen-treated pups both antenatally and postnatally showed vacuolization of the epithelial proximal tubules, interstitial edema, intratubular protein deposition but no significant glomerular changes. EM examination showed pleomorphic mitochondria and loss of microvilli in the tubules. The glomeruli showed extensive foot process effacement and irregularities of the glomerular basement membrane. EM changes were most marked in pups treated antenatally with ibuprofen, and indomethacin with gentamicin postnatally. Indomethacin, ibuprofen, and gentamicin cause significant change in glomerular and tubular structure in the neonatal rat model. U p to 5% of infants are delivered between 24 and 28 wk gestation, at a time when glomerulogenesis is occurring. Indomethacin and ibuprofen are commonly used in extremely premature neonates to close a patent ductus arteriosus at this time (1,2). Both of these drugs are successful in closing the ductus (3,4), but the morphologic effects these drugs may have on the developing kidney are unknown. Both drugs are known to be nephrotoxic, with indomethacin causing acute renal failure in 25% of premature neonates treated (5). Ibuprofen is considered to have less renal toxicity than indomethacin, but is as efficacious as indomethacin at closing the patent ductus (6). Two animal studies have shown an effect on glomerulogenesis by ibuprofen and a COX-2 selective inhibitor. In both studies, the number and size of glomeruli was decreased (7,8).Gentamicin is frequently administered at the same time as indomethacin or ibuprofen. Gentamicin has been shown in in vitro studies to affect nephron development (9). The combination of nonsteroidal anti-inflammatory drugs (NSAID) and gentamicin on glomerular development is unknown. The renal effect of indomethacin has not been examined in a neonatal animal model, nor has the combination of both indomethacin or ibuprofen and gentamicin.In the human, glomerulogenesis is complete at 36 wk gestation. The metanephron develops at 5 wk gestation, with vesicular glomeruli development occurring at 18 wk gestation. Glomerular tubular development occurs from 24 wk gestation and is complete at 36 wk (10 -12). In the rat model, glomerulogenesis continues after birth until 14 d of life (13). At birth the neonatal rat kidney is similar to that of a ...

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“…7,8,[13][14][15][16][17][18][19][20][21][22] Usually, the reported cases have been observed with prolonged use of these drugs-even topically-but they have also been reported shortly after initial intake. 2,14,15,18,21,[23][24][25] The average exposure time in most cases has been 5.4 months.…”

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confidence: 99%

Nephrotic Syndrome and Acute Tubular Necrosis Due to Meloxicam Use

et al. 2012

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Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used by patients all over the world. Five to eighteen percent of the patients who receive NSAIDs can suffer from kidney-related side effects. Among them, the most relevant are sodium and water retention, hyponatremia, worsening of hypertension or preexisting cardiac failure, hyperkalemia, acute kidney injury, chronic kidney disease, papillary necrosis, nephrotic syndrome (NS), and acute interstitial nephritis. We report the case of a 65-year-old woman who developed acute tubular necrosis and NS a few days after receiving 15 mg of meloxicam (MLX) for 3 days for tendinitis. Steroid therapy was begun with normalization of kidney function after 7 weeks of treatment. NS (minimal change disease) was characterized by frequent remissions and relapses as prednisone was lowered under 30 mg/day. Azathioprine (100 mg/day) was added on the fifth month of diagnosis and a complete remission was finally obtained 4 years after hospital admittance. In her last medical checkup, 8 years after her debut and receiving azathioprine (50 mg) and prednisone (5 mg/day), renal function was normal (creatinine 1.0 mg/dL and creatinine clearance 80 mL/min/1.73 m 2 ), proteinuria was 150 mg/day and there was no hematuria or hypertension. The aim of communicating this case is to raise a warning about these renal side effects of MLX. After thorough review of literature, only one other report with the same findings was found.

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Progression of Minimal-Change Glomerulopathy to Focal Glomerulosclerosis in a Patient with Fenoprofen Nephropathy

Cited by 15 publications

References 7 publications

Indomethacin, ibuprofen and gentamicin administered during late stages of glomerulogenesis do not reduce glomerular number at 14 days of age in the neonatal rat

Indomethacin, ibuprofen and gentamicin administered during late stages of glomerulogenesis do not reduce glomerular number at 14 days of age in the neonatal rat

Renal Glomeruli and Tubular Injury Following Indomethacin, Ibuprofen, and Gentamicin Exposure in a Neonatal Rat Model

Nephrotic Syndrome and Acute Tubular Necrosis Due to Meloxicam Use

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