Thursday, January 10, 2019

Topic Discussion: Secondary Oxalate Nephropathy


Oxalate deposition in the kidney is rare but recently several case reports have highlighted this finding.

A
recent KI reports paper summarized and did a systematic review of all published cases showing biopsy proven oxalate nephropathy.

In their systematic review, the most common presentation of oxalate nephropathy was acute kidney injury (35%), followed by acute on CKD (29%). Twenty-six percent of patients presented with kidney disease and stones, and 10% with CKD. In contrast, 20%–50% of patients with primary hyperoxaluria present with recurrent nephrolithiasis, and CKD or kidney failure. Proteinuria was the most common urinary finding (69%), followed by hematuria (32%). Urinary oxalate crystals were identified in only 26% of cases. 

What did the pathology show in most cases?  Kidney biopsy findings of acute tubular injury and interstitial infiltration were reported in 71% and 72% of patients, respectively, which suggested a cause role for the oxalate crystals. Majority of the patients had chronicity. Interestingly, glomerular changes were found in 59% of the biopsy specimens, which were mostly mesangial cellular proliferation; this might explain the high prevalence of proteinuria. There were no cases of crystal deposition in the glomeruli.
 
Renal replacement therapy is required in >50% of patients and most patients remain dialysis-dependent.  Monitoring the 24-hour urinary oxalate excretion rate might be a useful tool for prevention of oxalate nephropathy in high-risk patients.

Some of the causes the authors noted that could lead to secondary oxalate nephropathy were:

Pancreatic adenocarcinoma
Systemic sclerosis
Roux-en-Y bypass surgeries of various types
Hemicolectomy
Gastric bypass
Jejunoileal bypass
Bariatric surgery of various types
Cystic fibrosis
Orlistat( weight loss drug)
Octreotide
Mycophenolate mofetil ( rare)
Clostridium difficile colitis
Averrhoa carambola
Vitamin C
Peanuts
Tea
Rhubarb
Chaga mushroom
Piridoxylate
Crohn’s disease
Celiac disease
Absence of Oxalobacter formigenes colonization
Chronic pancreatitis
Small bowel resection
Diabetic gastroenteropathy

On twitter, I asked a question "
What determines why someone can develop oxalate nephropathy while someone else develops nephrolithiasis?"

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