Membranous glomerulonephritis natural history, complications and prognosis: Difference between revisions
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=== Secondary MN — === | === Secondary MN — === | ||
* In patients with secondary MN, cessation of the offending drug (eg, penicillamine, gold, or nonsteroidal anti-inflammatory drug) or effective treatment of the underlying disease is usually associated with improvement in the nephrotic syndrome. | |||
With penicillamine- or gold-associated disease, protein excretion may continue to rise for the first 1 to 12 months (mean 2 months) after the offending drug has been discontinued. | * With penicillamine- or gold-associated disease, protein excretion may continue to rise for the first 1 to 12 months (mean 2 months) after the offending drug has been discontinued. | ||
==References== | ==References== | ||
Revision as of 17:08, 16 July 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Ahsan Hussain, M.D.[2]
Overview
If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
OR
Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
OR
Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%. ==Natural History, Complications, and Prognosis==[1] [2]
Natural History
- The symptoms of Membranous glomerulonephritis usually develop in the fourth decade of life in males.
- The symptoms of membranous glomerulonephritis typically develop in young women increases the susceptibility of lupus.
Complications
- Common complications of membranous glomerulonepharitis include:
- Renal failure
Prognosis
- Spontaneous remission is most likely in women, children, those with lesser amounts of proteinuria, and adults under age 50 years with a normal serum creatinine concentration and benign histologic features.
- Although unproven, the rate of partial remission may be higher with the use of ACE inhibitors or ARBs.[3]
- Probability of progression — Based upon a study of 184 patients identified through the Toronto Glomerulonephritis Registry, a semiquantitative algorithm has been developed to predict the probability of progression to chronic kidney disease, which was defined as a creatinine clearance ≤60 mL/min per 1.73 m2.
- The probability of progression was assessed for those with 4, 6, and 8 g/day of proteinuria that persisted for 6, 9, 12, or 24 months.
- Multiple additional variables (including age, sex, serum creatinine, and creatinine clearance on presentation, serum albumin, presence of hypertension, rate of change of creatinine clearance, and therapy) were also tested to determine whether the predictive value provided by proteinuria could be improved. Of these variables, the initial creatinine clearance and the rate of change of clearance were the most useful predictors.
Based upon this approach, the best fitting logistic model utilized the following clinical characteristics:
●Persistent proteinuria for over six months
●Creatinine clearance upon presentation
●Slope of the decline in creatinine clearance over the assessed proteinuria period The addition of renal pathology as a variable had no effect on the performance of the model.
●The risk increases to 72 percent in the patient with proteinuria of 12 g/day, and a creatinine clearance on presentation of 96 mL/min, which declines to 78 mL/min by six months.
●Low risk –
* Proteinuria remains less than 4 g/day and creatinine clearance remains normal for a six-month follow-up period.
*Such patients have a less than 8 percent risk of developing chronic renal insufficiency over five years.
●Moderate risk –
Proteinuria is between 4 and 8 g/day and persists for more than six months. Creatinine clearance is normal or near normal and remains stable over six months of observation
. Chronic renal insufficiency develops over five years in approximately 50 percent of these patients.
●High risk –
●Acute bilateral renal vein thrombosis which may be associated with flank pain.
●Drug-induced acute interstitial nephritis, in which white cell, white cell casts, and possibly eosinophils are typically seen in the urine sediment.
●Superimposed crescentic glomerulonephritis, in which red cells and cellular casts are found in the urine sediment.
Secondary MN —
- In patients with secondary MN, cessation of the offending drug (eg, penicillamine, gold, or nonsteroidal anti-inflammatory drug) or effective treatment of the underlying disease is usually associated with improvement in the nephrotic syndrome.
- With penicillamine- or gold-associated disease, protein excretion may continue to rise for the first 1 to 12 months (mean 2 months) after the offending drug has been discontinued.
References
- ↑ Glassock RJ (July 2010). "The pathogenesis of idiopathic membranous nephropathy: a 50-year odyssey". Am. J. Kidney Dis. 56 (1): 157–67. doi:10.1053/j.ajkd.2010.01.008. PMID 20378220.
- ↑ Debiec H, Ronco P (July 2014). "Immunopathogenesis of membranous nephropathy: an update". Semin Immunopathol. 36 (4): 381–97. doi:10.1007/s00281-014-0423-y. PMID 24715030.
- ↑ Kerjaschki D (2000). "Pathogenetic concepts of membranous glomerulopathy (MGN)". J. Nephrol. 13 Suppl 3: S96–100. PMID 11132040.