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No Treatment?

October 4, 2011

The current issue of Journal of the American Society of Nephrology includes a “Brief Review” of Current Therapy for IgA Nephropathy. Floege and Eitner (of RWTH University of Aachen, Germany) point out that IgA nephropathy (henceforth IgAN) is a common cause of permanent kidney failure in many countries. Therapy of IgAN is based more on opinion than evidence at this point in time.

When experts get together to examine evidence and rate it, they produce a document based on the quality of the evidence supporting various treatment options. Recommendations are based on strong evidence, while suggestions are less supported.

They divide their “best opinion” approach by patient presentation:

  • The silent majority – 5 to 20% of kidneys from people “without kidney disease” show IgA deposits, suggesting that most patients never develop symptoms of the disorder. Over ten years, many patients with biopsy-proven IgAN show spontaneous remission of hematuria (blood in the urine); repeat kidney biopsy confirmed that IgA deposits were gone in many of these patients. Approximately one-third of these patients showed evidence of progressive disease, including the development of proteinuria (spot urine protein:creatinine ratio >1 mg/mg).
  • The typical patient – These patients have proteinuria and/or reduced estimated glomerular filtration rate (eGFR, a measure of how well the kidneys clear waste) and/or high blood pressure.
  • The atypical patient – presentation with either rapid loss of kidney function or with nephrotic syndrome (very heavy protein loss in the urine) may warrant early treatment with immunosuppressive agents because other kidney disorders may be present.
  • The transplant patient – IgAN may recur after transplantation; unfortunately, none of our current immunosuppressive agents prevent or treat this condition.

Click to enlarge

They present a nice algorithm for best suggested treatments (see figure). The silent majority warrant annual follow-up for at least 10 years to detect progression (proteinuria, falling eGFR, and/or high blood pressure) or spontaneous remission.

Other patients first warrant optimal supportive therapy:

  1. Control blood pressure with anti-angiotensin II drugs (converting enzyme inhibitors or receptor blockers) as first-line agents (the only treatment that will rise to the level of “recommended” in the pending KDIGO Clinical Practice Guideline for Glomerulonephritis). Encourage smoking cessation and weight loss, if overweight.
  2. Reduce dietary salt intake and/or add diuretics for edema control.
  3. Control each component of the metabolic syndrome, if present (obesity, high blood cholesterol, high blood glucose)
  4. Consider other supportive therapies, including aldosterone blockers, beta blockers, allopurinol, and/or sodium bicarbonate
  5. Other nonspecific measures to retard disease progression including avoiding nonsteroidal anti-inflammatory drugs (ibuprofen, naproxen) and controlling other abnormalities of blood chemistry, especially potassium and phosphorus.

Patients with eGFR of at least 30 mL/minute who show no reduction in proteinuria and/or a falling eGFR after 6 months of supportive treatment warrant a course of steroids. Two approaches have shown promise in this patient population, including a 6-month course that starts with oral prednisone 1 mg/kg body weight/day for 2 months followed by a reduction of 0.2 mg/kg/day monthly.

A variety of other therapies have been reported in small groups of patients; however, these treatments do not make the cut to even be suggested based on the evidence. These include fish oil, antiplatelet drugs, and tonsillectomy.

The authors also point out that several high-quality trials of treatments for IgAN will be completed in the coming years. Perhaps we will have strong enough evidence to make recommendations in the near future, rather than suggestions for mostly nonspecific treatments.

The bottom line: Most patients with IgAN have asymptomatic hematuria that resolves on its own after several years. Signs of progressive (or potentially progressive) disease include proteinuria, falling eGFR, and high blood pressure. If these develop, more follow-up and treatment will be necessary.


From → IgA Nephropathy

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  1. When Evidence Based Medicine Can’t Happen | Whizbang

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