Bheemanathi Hanuman Srinivas

Subcutaneous phaeohyphomycosis in kidney transplant recipients: A series of seven cases

Superficial and deep fungal infections are more frequent in transplant recipients primarily because of the failure of cell‐mediated immunity and lesser amount of antigen‐presenting Langerhans cells in their epidermis. Here, we report seven cases of post‐renal transplant subcutaneous phaeohyphomycosis, all of which manifested within 1 year after transplantation and were unresponsive to prolonged courses of itraconazole. This is the first case series, to our knowledge, of phaeohyphomycosis in transplant recipients in India.

Karyomegalic interstitial nephropathy following ifosfamide therapy

Ifosfamide (IFO), an alkylating agent used for the management of solid organ tumors, can cause reversible Fanconis syndrome and acute kidney injury. Karyomegalic interstitial nephropathy (KIN) is a rare form of chronic tubulointerstitial nephritis, initially described as a familial nephropathy in adults. So far, four cases of KIN have been reported in pediatric and adolescent population following treatment with IFO. We report a 22-year-old man who developed renal dysfunction following IFO therapy for relapsed Hodgkins lymphoma. Renal biopsy revealed chronic tubulointerstitial nephritis with atypical tubular epithelial cells showing nuclear enlargement and hyperchromasia, consistent with a diagnosis of KIN. The renal function improved following a short course of corticosteroids.

Acenocoumarol as an alternative anticoagulant in a patient with warfarin‐related nephropathy

Warfarin‐related nephropathy.

Dermoscopy of Langerhans cell histiocytosis

CLINICAL PRESENTATION An 11-month-old boy was brought by parents with 2-months’ history of asymptomatic rash over the trunk and neck associatedwith on-and-off fever. Cutaneous examination revealedmultiple discrete and grouped erythematous-to-skin-colored nonscaly papules of size varying from 1 3 1 mm to 3 3 3 mm over the trunk and neck (Fig 1). The child also had scalp scaling and generalized lymphadenopathy.

Cerebral venous thrombosis in a patient with acute postinfectious glomerulonephritis

Thrombosis of the cerebral venous sinuses (CVT) is described in nephrotic syndrome. A 13-year-old girl was admitted with acute post-infectious glomerulonephritis (APIGN). Subsequently she developed recurrent seizures with focal neurological deficits. On evaluation, she was found to have CVT. To the best of our knowledge, this is the first report of CVT in APIGN. Identifying this complication is imperative, as timely diagnosis and treatment could be lifesaving.

Acute infectious purpura fulminans caused by group A β-hemolytic Streptococcus: An uncommon organism.

132 Indian Dermatology Online Journal ‐ March‐April 2016 ‐ Volume 7 ‐ Issue 2 2005;53:1002‐9. 2. Gupta L, Naik H, Kumar NM, Kar HK. Granuloma faciale with extrafacial involvement and response to tacrolimus. J Cutan Aesthet Surg 2012;5:150‐2. 3. Gauger A, Ronet C, Schnopp C, Abeck D, Hein R, Köhn FM, et al. High local interleukin 5 production in granuloma faciale (eosinophilicum): Role of clonally expanded skin‐specific CD4+cells. Br J Dermatol 2005;153:454‐7.

Acute interstitial nephritis following viper bite: a rare association

Snake bite is a common cause of morbidity and mortality in rural India, accounting for an annual age-standardized mortality rate of 4.1/100 000 to 5.4/100 000, depending on the geographic location [1]. Renal failure is common following a viperidine bite; the majority of the patients develop acute tubular necrosis and a lesser number may develop cortical necrosis. Renal lesions apart from acute tubular necrosis and cortical necrosis are not well characterized in hemotoxic snake envenomation. Acute interstitial nephritis in the setting of hemotoxic envenomation is rare.

Vesiculobullous viral exanthem due to chikungunya in an infant

Sir, Chikungunya is an self-limiting arboviral disease caused by the chikungunya virus. It is transmitted mainly by the mosquito vectors Aedis aegypti and Aedis albopictus that breed in urban and semi-urban settings on clean standing (but stagnant) water.[1] Various dermatologic manifestations of chikungunya reported in infants include generalized erythema, maculopapular rash, vesiculobullous lesions, and skin peeling.[2] A 6-month-old child presented with high grade fever of three days and vesiculobullous rash of one day duration. Rash was initially erythematous and later turned dusky by the third day with associated blistering. Discrete, black flaccid vesicles and bullae were then noted on the trunk and perineum and spread to the extremities, sparing the face and mucosae [Figures ​[Figures11 and ​and2].2]. The child was otherwise unremarkable with no history of associated seizures, joint swelling, vomiting, or loose stools. There was no history of any medication intake prior to onset of blistering. Hemogram, liver function tests, renal function tests, and cerebrospinal fluid analysis were within normal limits. Blood culture and blister fluid culture were sterile. Serology for chikungunya by IgM antibody capture enzyme-linked immunosorbent assay (MAC-ELISA) (National Institute of Virology, Pune, India) was found to be positive from the serum sample sent on the sixth day of fever. An early vesicle was biopsied which on histopathological examination revealed intraepidermal bulla, dilated dermal blood vessels filled with fibrin and epidermal necrosis [Figure 3]. Child was treated symptomatically with paracetamol and fever subsided by the seventh day. Vesiculobullous rash started exfoliating by the sixth day and subsided completely without any pigmentary change by the tenth day. Figure 1 Purpuric vesicles and bullae over the trunk and extremities Figure 2 Purpuric vesicles and bullae over the gluteal region Figure 3 Histopathology of vesicle demonstrating intraepidermal cleft and dilated dermal blood vessels filled with fibrin and epidermal necrosis (H and E, ×100) In chikungunya, generalized erythematous rash develops abruptly during the first two days of fever followed by maculopapular rash in a centrifugal distribution on the second day of fever usually disappearing by the sixth day. Palms and soles are involved in around two-thirds of infants, but facial involvement is rare. Vesiculobullous eruptions in infants with chikungunya have been reported.[2,3,4] They usually present as sudden onset of flaccid vesicles and bullae usually on the fourth day of fever over the lower limbs that then spread to the perineum, abdomen, chest, and upper limb sparing the face and scalp. Lesions exfoliate by the sixth day and heal by the tenth day sometimes leaving behind pigmentary changes.[2] Clinical diagnosis can be confirmed by virus isolation, viral RNA by real-time polymerase chain reaction, virus specific immunoglobulin M antibodies by MAC-ELISA in a single serum sample collected in an acute state or four-fold increase in immunoglobulin G values in samples collected at least three weeks apart.[5] There is no specific antiviral therapy. Supportive treatment with paracetamol or other nonsalicylate analgesics is the mainstay of management. All suspected cases should be kept in mosquito nets during the febrile period and mosquito control measures should be adopted.[4] We report this case to highlight the interesting presentation of chikungunya in an infant in the form of vesiculobullous lesions. Chikungunya should be included in the differential diagnosis of febrile vesiculobullous eruption in infants.

Renal involvement in primary Sjogren’s syndrome: a prospective cohort study

The objective of the study is to prospectively evaluate the spectrum of clinical and subclinical renal involvement in patients with primary Sjogren’s syndrome (pSS). Of the 174 patients screened, seventy patients with pSS underwent renal function tests, urine examination, renal ultrasound, arterial blood gases, urine pH followed by urine acidification test and renal biopsy (if indicated). Renal tubular acidosis (RTA) was treated with alkali replacement and moderate–severe tubulointerstitial nephritis (TIN) was treated with oral prednisolone. Sixty-two patients completed 1-year follow-up. A comparison was made between patients with and without renal involvement. Thirty-five (50%) patients had renal involvement. They had a lower baseline eGFR (71.85 ± 18.04 vs. 83.8 ± 17, p = 0.005). Twenty-nine patients had RTA (25 complete and 4 incomplete). Eleven patients had urinary abnormalities. Patients with RTA (n = 29) were younger (34.9 ± 9 vs. 42 ± 11.3, p = 0.006), had fewer articular (34% vs. 78%, p = 0.001) and ocular sicca (62% vs. 88%, P = 0.01) than those without RTA (n = 41) and commonly presented with hypokalemic paralysis. On biopsy, TIN (9/17) and IgA nephropathy (3/17) were most common. On follow-up, there was no clinically significant change in eGFR; however, one patient with renal calculi and incomplete distal renal tubular acidosis (dRTA) progressed to complete dRTA. Two patients treated with steroids had marginal improvement in eGFR. Renal involvement in pSS is under-recognized with the most common manifestation being RTA presenting with hypokalemic paralysis. These patients are younger with less articular and sicca symptoms. Subclinical RTA may progress to complete RTA. Renal biopsy should be considered in all patients with renal involvement.

Severe acute kidney injury owing to rhabdomyolysis and intravascular haemolysis in an 11-year-old child with G6PD deficiency

Abstract Glucose-6-phosphate dehydrogenase (G6PD) deficiency leading to acute intravascular haemolysis and acute kidney injury (AKI) is a known clinical presentation. However, there is a paucity of information regarding the occurrence of rhabdomyolysis and myoglobinuria in G6PD-deficient individuals, especially children. An 11-year-old south Indian Tamil girl presented with severe anaemia and anuric AKI following a short febrile illness. Investigations demonstrated evidence of intravascular haemolysis and rhabdomyolysis, and on histopathology myoglobin deposits (casts) were detected in the renal tubules. She was successfully managed with repeated sessions of haemodialysis and blood transfusions. Follow-up estimation of G6PD levels after 3 months confirmed severe G6PD deficiency (0.003 nkat/g haemoglobin). Although there are anecdotal reports of myoglobinuria in G6PD-deficient individuals, the occurrence of severe anuric AKI in this clinical setting has not been reported. It can be speculated that myoglobinuria (in addition to haemoglobinuria) can contribute towards jeopardising renal function in G6PD deficiency-related acute haemolytic crisis.