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Visual disturbances are common in patients who received renal transplant. Visual acuity is reduced in 60% of renal transplant patients after 10‑year posttransplant. The most common causes are cataracts, diabetic retinopathy, and hypertensive retinopathy. However, infectious causes of visual loss are rare and most commonly associated with cytomegalovirus and toxoplasmosis infections. Here, we report a 32‑year‑old male who developed visual loss 6 months after receiving a live‑related kidney transplant. The patient had a history of varicella infection in the immediate posttransplant period. The visual loss was secondary to acute retinal necrosis probably secondary to a Varicella infection. This rare manifestation is even more unique in a posttransplant scenario which is usually associated with progressive outer retinal necrosis. The patient had developed irreversible visual loss secondary to the retinal necrosis. Here, we report this rare association as well as 2‑year ophthalmological follow‑up of this patient. [ABSTRACT FROM AUTHOR]

The incidence of colon perforation in the posttransplant period is 1.3% based on various single‑center studies. We report the case of a 32‑year‑old male, a known case of chronic kidney disease and end‑stage renal disease who received a live‑related ABO‑compatible transplant. The patient was started on tacrolimus, mycophenolate mofetil, and steroids; no induction was given. The patient had a delayed graft function, and his creatinine was persistently high. Hence, a biopsy was done on postoperative day 4, which revealed an acute tubular injury with features of calcineurin inhibitor toxicity. His tacrolimus dose was reduced and his output improved until day 13, after which his renal function worsened. The repeat tacrolimus level was low. Hence, the patient was started on pulse steroids and discharged after the patient improved symptomatically (discharge creatinine: 2.1). The patient was readmitted 3 days after discharge with severe abdominal pain. The patient’s blood pressure was 90/30 mmHg; he was drowsy and tachypneic. His abdomen was distended. Computed tomography of the abdomen revealed pneumoperitoneum, and the patient was subjected to an explorative laparotomy. There was colonic perforation. The peritoneum and colon revealed multiple punched‑out lesions and a right hemicolectomy was done. A biopsy revealed suppurative inflammation involving all three layers with multiple giant cells, and tissue staining revealed ribbon‑like aseptate hyphae with 90° angulation suggestive of mucormycosis. The patient expired in the immediate postoperative period. The final diagnosis of mucormycosis‑associated colon perforation was made. Only one such case has been reported previously. [ABSTRACT FROM AUTHOR]

Primary focal segmental glomerulosclerosis (FSGS) recurrence varies between 10% and 60% and is an important predictor of graft survival. Here, we report the case with a combination of recurrence of FSGS, acute cell‑mediated rejection, and donor‑derived immunoglobulin A(IgA) nephropathy which required treatment with plasmapheresis and antithymocyte globulin. This patient is an 18‑year‑old female whose native kidney disease was a biopsy‑proven FSGS and underwent ABO compatible live‑related renal transplant with her mother as a donor. No induction agents were given and the patient was put on triple immunosuppression with Calcineurin inhibitors (CNIs), Mycophenolate mofetil (MMF), and steroids. On postoperative Day 2, the patient developed nephrotic range proteinuria. Atransplant kidney biopsy was done. Biopsy revealed acute cell‑mediated rejection, Banff II A with i3, t3, ptc1, v1, and C4d negative. There was also an increase in mesangial cellularity with IgA 3+ and C3 1+ on immunofluorescence which is IgA nephropathy, likely donor derived. Electron microscopy revealed significant effacement of podocytes. CNI levels are adequate. Pulse methylprednisolone 5 doses given. The patient was given two sessions of plasmapheresis with albumin and a single dose of rabbit antithymocyte globulin (ATG) 1.5 mg/kg was given. Plasmapheresis was withheld in view of studies reporting the removal of ATG following plasmapheresis. There was a gradual worsening of renal function with peak serum creatinine of 9 mg/dL which required three sessions of hemodialysis. The second renal biopsy on Day 13 showed features of acute tubular injury with borderline changes suspicious of acute cell mediated rejection (ACMR)–i1, t1. Currently, the patient is on regular follow‑up with normal renal function with urine polymerase chain reaction of 0.4. We report this case which presented with a puzzling combination of ACMR, possible recurrence of native disease, and likely donor‑derived IgA nephropathy that provided us with challenges in management. Treatment protocols with optimal dosing strategies and assessing response to treatment in these situations are still unclear due to the lack of large randomized trials. [ABSTRACT FROM AUTHOR]