Infection occurs commonly after renal transplantation, and it is associated with significant morbidity and mortality. Infections are commonly associated with changes in the white blood cell count; however, it may be masked in the background of immunosuppression. Immunosuppression modulation during infection is crucial, keeping in mind, the risk of rejection on the one hand and risk of severe infection and mortality on the other hand. Idea about timeline of infection after renal transplantation in a particular geographical area is helpful in management of infection. The approach to modulate immunosuppressive agents will vary depending on the severity of infection. Many infections require specific anti-infective agents which may have significant drug interaction with immunosuppressive agents. It may also necessitate stoppage of immunosuppression either temporarily or permanently in severe infections to salvage the life of the patient.

Introduction: Kidneys are the most frequently transplanted organs; renal transplantation is the preferred method for treating patients with chronic kidney disease; and posttransplantation urinary tract infection (UTI) is still a source of morbidity and graft failure. Materials and Methods: This prospective study was conducted during the period of August 2016 to February 2018. A total of 35 renal transplant recipients were included in the study. Results: The most common symptom associated with the infection was dysuria (71%). Only 66% of the cases were febrile. Almost 17% of the cases presented with shock. Urine culture was positive in 23 (65%) cases, with bacteria in 22 (96%) and fungus in 1 (4%). Predominant bacteria grown from cultures were Klebsiella pneumoniae 32%, Pseudomonas aeruginosa 18%, Escherichia coli 14%, Enterococcus faecalis 13%, Acinetobacter 10%, Staphylococcus aureus 9%, and Enterobacter 4%. Antibiotic resistance profiles showed a high resistance patterns to ceftriaxone 60%, levofloxacin 53%, nitrofurantoin 53%, ciprofloxacin 40%, cotrimoxazole 40%, piperacillin–tazobactam 26%, amikacin 26%, gentamicin 26%, meropenem 26%, and imipenem 13%. Patients were followed up over a period of 4 weeks. At the 2^nd week of follow-up, 2 (5%) cases were still culture positive, and the symptoms of UTI persisted in 6 (17%) cases. Of 35 cases, 25 were followed up till the 4^th week. Culture positive was noted in 6 (24%) cases, and the symptoms persisted in 10 (40%) cases. In recurrent infections, relapses were noted in 3 (50%) cases and reinfections in 3 (50%). Conclusion: In these high-risk patients, antibiotic selection, duration, and stewardship need to be readdressed. Microbial profile and sensitivity patterns in such patients are different from the usual UTIs.

Parvovirus (PV) infection is a rare cause of persistent anemia in kidney transplant recipients. The diagnosis of PV infection depends on a high index of suspicion, persistent anemia, red cell aplasia in the bone marrow, and positive polymerase chain reaction for PV B19. Treatment with intravenous immunoglobulin (IVIg) has shown to improve anemia but persistence of PV is common after treatment. This case report highlights a postkidney transplant recipient who had PV infection, treated with IVIg but had multiple relapses. He was managed with monthly IVIg prophylactic therapy for 6 months following which he had complete clearance of PV. PV B19 results in multiple relapses in postkidney transplant patients. Monthly prophylaxis therapy with higher dose delivery of IVIg can result in the clearance of PV and relapse-free response. Further studies may be required to determine the duration of prophylaxis therapy.

A 60-year-old male patient, who is a known case of end-stage kidney disease postliving donor renal transplantation on triple maintenance immunosuppression, presented with persistent dyspeptic symptoms 8 months posttransplant, not relieved with prolonged proton-pump inhibitor therapy. On endoscopy, found to have large ulcerated nodular lesion in the body of stomach suggestive of malignancy. On biopsy, it was diagnosed with primary gastric tuberculosis (TB). Complete clinical and endoscopic resolution was achieved following anti-TB treatment.