Granulomatous Interstitial Nephritis after a Jejunoileal Bypass: An Ultrastructural and Histochemical Study

Verani, Regina; Nasir, Marwan A.; Foley, Richard J.

doi:10.1159/000167935

Cited by 15 publications

(9 citation statements)

References 4 publications

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“…Earlier institution of these dietary interventions may have been more successful. Similar poor outcomes were reported for patients with oxalate nephropathy after JI bypass (4), except for a few patients in whom surgical reversal of bypass was performed and resulted in improvement of renal function (5,27). None of the patients in our study had surgical reversal of RYGB, and whether this would have led to renal function improvement is unknown.…”

Section: Discussionsupporting

confidence: 77%

Oxalate Nephropathy Complicating Roux-en-Y Gastric Bypass

Nasr

D’Agati

Said

et al. 2008

Clinical Journal of the American Society of Nephrology

183

143

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Background and objectives: The most common bariatric surgery is Roux-en-Y gastric bypass (RYGB), which has been associated with hyperoxaluria and nephrolithiasis. We report a novel association of RYGB with renal insufficiency as a result of oxalate nephropathy.Design, setting, participants, & measurements: Eleven cases of oxalate nephropathy after RYGB were identified from the Renal Pathology Laboratory of Columbia University. The clinical features, pathologic findings, and outcomes are described.Results: Patients were predominantly white (72.7%) with a mean age of 61.3 yr. Indications for RYGB included morbid obesity (eight patients) and reconstruction after total gastrectomy for gastric cancer (three patients). All 11 patients had a history of hypertension, and 9 were diabetic. Patients presented with acute renal failure, often superimposed on mild chronic renal insufficiency (n ‫؍‬ 7), at a median of 12 mo after RYGB. The mean creatinine at baseline, at discovery of acute renal failure, and at biopsy was 1.5, 5.0, and 6.5 mg/dl, respectively. Renal biopsies revealed diffuse tubular degenerative changes, abundant tubular calcium oxalate deposits, and varying degrees of tubulointerstitial scarring. In addition, seven biopsies had underlying diabetic glomerulosclerosis and two had glomerulosclerosis attributable to obesity and hypertension. Eight of 11 patients rapidly progressed to ESRD and required hemodialysis at a mean of 3.2 wk after renal biopsy. The remaining three patients were left with significant chronic kidney disease.Conclusions: Oxalate nephropathy is an underrecognized complication of RYGB and typically results in rapid progression to ESRD. Patients with pre-existing renal disease may be at higher risk for this complication.

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Section: Discussionsupporting

confidence: 77%

Oxalate Nephropathy Complicating Roux-en-Y Gastric Bypass

Nasr

D’Agati

Said

et al. 2008

Clinical Journal of the American Society of Nephrology

183

143

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“…The hyperoxaluria can be severe and can result in kidney failure. In selected older case reports, oxalate nephropathy stabilized or improved after reversal of jejunoileal bypass surgery 23, 24 . Oxalate hyperabsorption can also result from medications such as orlistat that interfere with fat absorption from the gastrointestinal tract 25 .…”

Section: Secondary Hyperoxaluriamentioning

confidence: 99%

Update on Oxalate Crystal Disease

et al. 2013

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Oxalate arthropathy is a rare cause of arthritis characterized by deposition of calcium oxalate crystals within synovial fluid. This condition typically occurs in patients with underlying primary or secondary hyperoxaluria. Primary hyperoxaluria constitutes a group of genetic disorders resulting in endogenous overproduction of oxalate, whereas secondary hyperoxaluria results from gastrointestinal disorders associated with fat malabsorption and increased absorption of dietary oxalate. In both conditions oxalate crystals can deposit in the kidney leading to renal failure. Since oxalate is primarily renally eliminated, it accumulates throughout the body in renal failure, a state termed oxalosis. Affected organs can include bones, joints, heart, eyes and skin. Since patients can present with renal failure and oxalosis before the underlying diagnosis of hyperoxaluria has been made, it is important to consider hyperoxaluria in patients who present with unexplained soft tissue crystal deposition. The best treatment of oxalosis is prevention. If patients present with advanced disease, treatment of oxalate arthritis consists of symptom management and control of the underlying disease process.

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“…By light microscopy, granulomatous interstitial nephritis characteristically shows clusters or collections of epithelioid histiocytes, with varying numbers of small lymphocytes and sometimes multinucleated giant cells. Caseous necrosis generally occurs only in patients with mycobacterial or fungal infections (Mignon et al, 1984;Cohen, 1986;Schwarz et al, 1988;Verani et al, 1989;Hannedouche et al, 1990;Lien et al, 1993). Immunofluorescence and electronmicroscopy are generally not helpful, but a special stain for organisms, including Ziehl-Neilson, PAS, or Grocott's silver stains, should be performed on all of these cases.…”

Section: Granulomatous Interstitial Nephritismentioning

confidence: 99%

Chemical-Induced Nephropathy: A Review of the Renal Tubulointerstitial Lesions in Humans

Silva¹

2004

Toxicol Pathol

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It is almost ironic that one of the major organs that serves to maintain the "internal milieux" by secretion of various toxic agents, can itself become injured in the process. The pattern of morphologic renal injury is nonspecific and can involve any of the components of the kidney, although the injury and subsequent morphologic changes are most commonly noted in the tubules and/or interstitium. Of course, unless the drug/toxin is commonly or regularly noted to be associated with tubular and/or interstitial injury, the association of the drug with the renal changes may be missed and the correlation may not necessarily identify causation. For example, if a drug is associated with a renal injury in a given individual, it may be quite difficult to prove that the drug is the cause of the injury. This scenario is somewhat reminiscent of the test question-is it "true-true-related," or "true-true-unrelated"? Sometimes it is only by the accrual of a great many examples or correlations, and or dissection of the pathophysiology, can it be shown that the drug is directly related to the observed morphologic (and subsequent clinical) injury. Renal changes induced by chemicals can affect the tubules, interstitium or both. This review of chemically induced nephropathy in humans considers acute tubular necrosis, interstitial nephritis, and tubulointerstitial nephritis or nephropathy. Because the tubules and the interstitium are so intimately related, injury to 1 of these 2 components may eventually lead to injury of the other, resulting in tubulointerstitial disease.

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Granulomatous Interstitial Nephritis after a Jejunoileal Bypass: An Ultrastructural and Histochemical Study

Cited by 15 publications

References 4 publications

Oxalate Nephropathy Complicating Roux-en-Y Gastric Bypass

Oxalate Nephropathy Complicating Roux-en-Y Gastric Bypass

Update on Oxalate Crystal Disease

Chemical-Induced Nephropathy: A Review of the Renal Tubulointerstitial Lesions in Humans

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