Immunoglobulin A Nephropathy and Malaria falciparum Infection; a Rare Association
A 28-year-old man visited the Al-Zahra Hospital in Isfahan, Iran on September 2011, because of persistent fever for one month despite repeated use of antipyretics. The patient was an engineer who had come back from a work mission in Sudan. After 30 days of working in Sudan, he developed fever, chills, malaise and abdominal pain. In his past medical history, he had an open right ureterolithotomy 4 years earlier. The patient had, hematemesis and dysuria, not responding to medical therapy there.\nUpon admission, the patient was dehydrated and lethargic and had fever. He also had hematuria. Initial laboratory tests showed the following values: hemoglobin: 9.0 g/dl and serum creatinine: 1.9 mg/dl. Urine dipstick examination showed hematuria (2+) and proteinuria (2+). In kidney sonography, right kidney dilation and pus accumulation in the collecting system (pyonephrosis) was detected that was confirmed by CT. Based on his past history, we assumed that a ureteral stricture had occurred after the stone surgery, culminating in hydronephrosis and then, pyonephrosis. Despite the administration of wide spectrum antibiotics (meropenem 1g IV Tid, plus vancomycin) and right kidney nephrostomy, fever was not subsided and general condition was not improved. Upon placing the nephrostomy, 200 mL of pus was drained that in culture, showed the growth of pseudomas aeroginosa, and antibiotic changed to meropenem and amikacin. A repeat CT after nephrostomy showed focal pyelonephritis (lobar nephronia); therefore, the patient underwent nephrectomy. Examination of the tissue revealed significant inflammatory infiltration consisting of mononuclear and polynuclear cells were indentified, consistent with pyonephrosis. Also renal structures were destructed profoundly (). Before contemplating nephrectomy, a peripheral blood smear had been performed as a part of the sepsis work-up that showed hyperparasitemia with Plasmodium falciparum.\nAnti-malarial treatment on the base of national protocol including aresunate and fansidar was initiated immediately. Fever and other symptoms subsided and general condition became better, and serial peripheral blood smears showed low and negative parasite at third and seventh days after treatment. However, the patient had a serum creatinine up to 1.6 mg/dl at the time of discharge. Around one year after discharge, the patient was symptom free, and for further evaluation of mild renal failure, patient was referred to the clinic of nephrology (in November 2012). Primary work up revealed that the patient had a serum creatinine of 1.7mg/dl (eGFR# 75cc/min). Urine examination showed dysmorphic hematuria. In addition, there was a 500mg/day proteinuria. In further history taking, we noticed to serum creatinine of 0.8mg/dl with normal urine analysis prior to trip to Sudan, one year ago.\nTo find out the etiology of renal failure with proteinuria, a left kidney biopsy was conducted. In immunofluorescence (IF) study, prominent deposit of IgA antibody (3+ on a score of 0 to 3+) was detected .There was also 2+ deposit of C3. However, there was not C1q deposits. In light microscopy, mesangial proliferation in around 50% of the glomeruli was observed. In addition, there was a slight mesangial area thickness (). Tubules were closely packed and the interstitium was normal. However, RBC in tubules was very popular. Endocapillary or extracapillary proliferation was absent. Prominent deposit of IgA antibody along with C3 deposits and absence of C1q in IF study was interpreted as IgA nephropathy and according to the Oxford classification for this nephropathy, and biopsy was classified as M1E0S0T0(–). The patient was prescribed by a combination of low dose prednisolon and angiotensin converting enzyme inhibitor. Six months after treatment, serum creatinine decreased to 1.3mg/dl and urine abnormalities were disappeared.