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Background: Tetralogy of Fallot is the most common cyanotic congenital heart disease. Patients with the condition have a high risk of developing chronic kidney disease. Treatment of kidney disease in patients with complex hemodynamics presents unique challenges. However, there are very few reports on the treatment of end-stage renal failure in patients with tetralogy of Fallot. Case presentation: We present a rare case of peritoneal dialysis in a 47-year-old man with tetralogy of Fallot who had not undergone intracardiac repair. Peritoneal dialysis successfully removed fluids and solutes without adversely affecting the patient's hemodynamics. Our patient was managed with peritoneal dialysis for 5 years before he succumbed to sepsis secondary to digestive tract perforation. Conclusions: In this paper, we discuss the importance of monitoring acid-base balance, changes in cyanosis, and hyperviscosity syndrome during peritoneal dialysis in patients with tetralogy of Fallot. Lower leg edema and B-type natriuretic peptide level were useful monitoring parameters in this case. This case illustrates that with attention to the patient's unique requirements, peritoneal dialysis can provide successful renal replacement therapy without compromising hemodynamics in patients with tetralogy of Fallot.

Background: Carbamazepine-induced acute kidney injury is mainly caused by acute tubulointerstitial nephritis. Only one case of carbamazepine-induced eosinophilic granulomatosis with polyangiitis (EGPA) with acute kidney injury has been reported. But the patient's condition improved with the immediate discontinuation of carbamazepine. We present a case requiring hemodialysis and steroid therapy for carbamazepine-induced EGPA with acute kidney injury. Case presentation: A 77-year-old man with allergic rhinitis was prescribed carbamazepine for trigeminal neuralgia 1 year ago. He developed rash and itching on the left forearm 1 month ago and was diagnosed with polymorphic exudative erythema and admitted to our hospital. Laboratory data revealed leukocytosis eosinophilia and renal failure (serum creatinine 9.2 mg/dL). Carbamazepine was discontinued, and hemodialysis was initiated because of acute uremia and oliguria. A lymphocyte stimulation test for carbamazepine was positive. Polyneuropathy in the upper and lower extremities was observed by electromyogram, and a renal biopsy indicated EGPA. The main clinical findings were allergic rhinitis, eosinophilia, and vasculitis symptoms, such as multiple mononeuritis and muscle weakness. Renal biopsy showed diffuse cellular infiltration dominated by eosinophils in the interstitium, with granulomatous changes in particular observed around the arteriole. Fibrinoid necrosis was also observed around the arteriole. We therefore made a diagnosis of carbamazepine-induced EGPA. Following steroid therapy after the discontinuation of carbamazepine, the patient was discharged from our hospital without hemodialysis. In contrast with the previous case of EGPA, the present case had the following characteristics: (1) elderly male patient, (2) hemodialysis required for acute kidney injury, and (3) improved renal function following steroid therapy after discontinuation of carbamazepine. Conclusion: Our case report indicates that early diagnosis and appropriate therapy can improve acute kidney injury caused by carbamazepine and allow the patient to discontinue dialysis.

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Recently, the comprehensive concept of “infection-related glomerulonephritis (IRGN)” has replaced that of postinfectious glomerulonephritis (PIGN) because of the diverse infection patterns, epidemiology, clinical features, and pathogenesis. In addition to evidence of infection, hypocomplementemia particularly depresses serum complement 3 (C3), with endocapillary proliferative and exudative GN developing into membranoproliferative glomerulonephritis (MPGN); also, C3-dominant or co-dominant glomerular immunofluorescence staining is central for diagnosing IRGN. Moreover, nephritis-associated plasmin receptor (NAPlr), originally isolated from the cytoplasmic fraction of group A Streptococci, is vital as an essential inducer of C3-dominant glomerular injury and is a key diagnostic biomarker for IRGN. Meanwhile, “C3 glomerulopathy (C3G)”, also showing a histological pattern of MPGN due to acquired or genetic dysregulation of the complement alternative pathway (AP), mimics C3-dominant IRGN. Initially, C3G was characterized by intensive “isolated C3” deposition on glomeruli. However, updated definitions allow for glomerular deposition of other complement factors or immunoglobulins if C3 positivity is dominant and at least two orders of magnitude greater than any other immunoreactant, which makes it challenging to quickly distinguish pathomorphological findings between IRGN and C3G. As for NAPlr, it was demonstrated to induce complement AP activation directly in vitro, and it aggravates glomerular injury in the development of IRGN. A recent report identified anti-factor B autoantibodies as a contributing factor for complement AP activation in pediatric patients with PIGN. Moreover, C3G with glomerular NAPlr deposition without evidence of infection was reported. Taken together, the clinico-pathogenic features of IRGN overlap considerably with those of C3G. In this review, similarities and differences between the two diseases are highlighted.