scholarly journals Rapidly progressive renal failure--a rare presentation of granulomatous interstitial nephritis due to tuberculosis--case report and review of literature

2011 ◽  
Vol 4 (6) ◽  
pp. 383-385 ◽  
Author(s):  
A. Kaul ◽  
R. K. Sharma ◽  
J. Krishnasamy ◽  
V. Ruhela ◽  
N. Kumari
1993 ◽  
Vol 48 (2) ◽  
pp. 115-118 ◽  
Author(s):  
M. Meysman ◽  
J. Sennesael ◽  
P. Vanderniepen ◽  
K. Vanden Houte ◽  
E. Pierre ◽  
...  

2005 ◽  
Vol 37 (3) ◽  
pp. 561-564 ◽  
Author(s):  
Sandeep Mahajan ◽  
Vikram Kalra ◽  
A. K. Dinda ◽  
S. C. Tiwari ◽  
S. K. Agarwal ◽  
...  

2021 ◽  
pp. 004947552110199
Author(s):  
Parvati Joshi ◽  
Saurabh Nayak ◽  
Mudalsha Ravina ◽  
Archana Keche ◽  
Vinay Rathore

Parasitic infections do not usually present with rapidly progressive renal failure but can provoke glomerular lesions which are mostly proliferative. In filarial infection, glomerular involvement is usually mild and transient, and presentation with renal failure is rare. We report occult filariasis presenting as rapidly progressive renal failure due to immune-complex mediated membranoproliferative glomerulonephritis. Our patient responded to treatment with diethylcarbamazine and a short course of steroid. This case highlights the importance of thorough workup to identify the cause and consideration of filariasis in an endemic area.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Wenbo Zhao ◽  
Xinxin Ma ◽  
Xiaohao Zhang ◽  
Dan Luo ◽  
Jun Zhang ◽  
...  

Abstract Background Heterozygous mutations in the inverted formin 2 (INF2) gene are related to secondary focal segmental glomerulosclerosis (FSGS), a rare secondary disease associated with rapidly progressive renal failure. Case presentation We report a patient with familial autosomal INF2 mutation manifesting nephritic syndromes and elevated serum creatinine levels. Mutational analysis revealed an autosomal dominant (AD) inheritance pattern and a mutation in exon 4 (p.Arg214Cys) of INF2 as the likely cause, which has not been previously described in an Asian family. The patient progressed to end-stage renal disease (ESRD) and received hemodialysis. His mother had undergone renal transplant 3 years earlier, and his grandmother had carried the p.Arg214Cys mutation for more than 80 years without any sign of renal dysfunction. Conclusions This is the first report to identify an association between a familial autosomal dominant INF2 p.Arg214Cys mutation and rapidly progressive renal disease in an Asian family. INF2 mutation analysis should not be restricted to individuals without family history of FSGS, rather it should also be performed on individuals for whom drug-based therapies are not effective. In this case, kidney transplant is an effective alternative.


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