Ratan Jha

Acute pancreatitis following kidney transplantation – role of viral infections

Abstract: Acute pancreatitis following renal transplantation is an unusual complication that carries a high mortality. Over the last 10 yr, five of 185 patients at our center developed acute pancreatitis. All had live related donors and were on conventional triple drug immunosuppression. Pancreatitis was classified according to the computed tomography scan based on Atlanta Classification. All five patients who developed acute pancreatitis had evidence of symptomatic or serologically active viral infection (chicken pox in two, cytomegalovirus infection in two, hepatitis E virus in one) and no patient without viral infection developed pancreatitis. Overall, 45 patients developed symptomatic or serologically active viral infection. There was a significant association between viral infection and pancreatitis (chi‐square test, p < 0.001). Three patients with severe acute pancreatitis died while both patients with mild pancreatitis survived. An active search for viral infections should be made in all patients with acute pancreatitis. Specific antiviral measures may help reduce the mortality of acute pancreatitis in these patients. Consideration must be given to varicella immunization in patients with renal failure.

Central pontine myelinolysis following ‘slow’ correction of hyponatremia

Two patients with central pontine myelinolysis are described for the peculiar mode of development. Both patients were in chronic renal failure and admitted in a stuporous state due to hyponatremia. Both developed central pontine myelinolysis during the hospital stay following slow and judicious correction of hyponatremia. The role of chronicity of hyponatremia prior to its correction, in the genesis of central pontine myelinolysis, particularly in the patients who have chronic debilitating illness, septicemia or malnutrition, is highlighted.

Granulocyte macrophage colony stimulating factor (GM-CSF) induced sero-protection in end stage renal failure patients to hepatitis B in vaccine non-responders.

Hepatitis B (HB) virus infection is a major health problem in dialysis dependent end stage renal failure (ESRF) patients. The sero-conversion rate after recombinant HB vaccine in ESRF patients is poor. Adjuvants like Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) have been found to improve response rate to vaccines. This study was conducted to evaluate the efficacy of GM-CSF as an adjuvant to HB vaccine in ESRF patients who were non-responders to the usual three double dose vaccinations (primary non-responders). Fifty consecutive HBsAg negative and anti-HBs negative ESRF patients on hemodialysis over thirty months were prospectively included (Jan. 96-June 98). All received 40 ug of recombinant HB vaccine at 0, 1, 2 month interval. Anti-HBs titres were subsequently tested after four weeks of the third dose. There were 19 (38%) primary non-responders (antiHBs negative). Twelve (Group I) of primary non-responders were given an additional dose of HB vaccine with 300 ug (5–6 ug/kg) of GM-CSF (Leucomax) and the remaining seven (Group II) received only an additional dose of HB vaccine. Anti-HBs was determined by Abbotts ELISA kit, and titre above 10 m IU/mL was considered as protective. In Group I, sero-protective titres were obtained in 11 out of 12 (91.6%) patients, whereas in Group II none of the patients achieved sero-protection (p < 0.001). The sero-conversion rate improved from initial 62% (31/50) to overall 84% (42/50) after the use of GM-CSF. There were no adverse events noted with the use of GM-CSF. At one year, 24 out of 32 (75%) who were sero-protected earlier continued to remain sero-protected. This study indicates that GM-CSF is a potent HB vaccine adjuvant for sero-conversion in primary non-responders.

Visceral Leishmaniasis in a Renal Transplant Recipient: Diagnostic and Therapeutic Problems

Visceral leishmaniasis is infrequently reported in renal transplant recipients. A 40-year-old renal transplant recipient developed hepatosplenomegaly and pyrexia of unknown origin 5 months after transplantation. Visceral leishmaniasis was confirmed on bone marrow examination. The usual dose of antiparasitic therapy with stibogluconate sodium failed to eradicate Leishmania donovani. High-dose conventional therapy with stibogluconate sodium for an extended period of time was successful in the treatment of a relapse of leishmaniasis.

Acquired perforating dermatoses in patients with diabetic kidney disease on hemodialysis.

Acquired perforating dermatoses (APD) is an uncommon skin disorder seen in patients with diabetes mellitus, chronic kidney disease, or both together. We present the clinicopathological features of APD in patients with diabetic kidney disease and discuss the recent advances in management. We retrospectively analyzed the data of 8 patients with APD presenting to our center. All patients were known cases of Type 2 diabetes and chronic kidney disease requiring maintenance dialysis. Acquired perforating dermatoses was diagnosed based on clinical presentation of itchy, keratotic papulonodular lesions, and characteristic histopathological features of transepithelial elimination on skin biopsy. The patients were subdivided into 4 types of APD based on the biopsy features. All our patients had Type 2 diabetes over 5 years duration and were on maintenance dialysis for more than 6 months before presentation. Acquired perforating dermatoses symptoms appeared 2 to 6 months before presentation. The majority of patients (6/8) had a subtype of reactive perforating collagenosis. All the patients showed significant resolution with topical glucocorticoid therapy. Acquired perforating dermatoses is a skin complication seen in Type 2 diabetes, chronic kidney disease, or when both are present together. Early identification and therapy prevents the associated morbidity.

Acute kidney injury following cardiac surgery

Acute kidney injury (AKI), a recognized complication of cardiac surgery with cardiopulmonary bypass (CPB) is associated with increased morbidity and mortality (15-30%) with approximately 1% of all the affected patients requiring dialysis. Early detection of AKI would enable intervention before occurrence of irreversible injury and might minimize the morbidity and mortality. Recently developed biomarkers of AKI facilitate its earlier discovery and help assessment of its severity and prognosis. In this article, we review the causes of well-known yet inexplicable association between CPB and AKI, the advances in pathophysiologic basis, the diagnostics and the management options.

Carbon Monoxide Poisoning: An Unusual Cause of Acute Renal Failure

Carbon monoxide poisoning in a family of 3 persons resulted in renal failure with neurological damage in a 40-year-old husband and a fatal neurological injury in 35-year-old wife whereas the newborn child survived without any ill effects. Rhabdomyolysis and myoglobinuria secondary to anoxia was the probable cause of acute renal failure. The recognition of nontraumatic rhabdomyolysis-related acute renal failure is important in preventing fatality if neurological salvage is done at the right time.

Primary hyperparathyroidism: Achanging scenario in India

Introduction: Primary hyperparathyroidism (PHPT) is largely a symptomatic disease with varied systemic manifestations, complicated by coexisting Vitamin D (Vit D) deficiency. Increasing awareness, developments in diagnostics, and Vit D supplementation may have an impact on the disease profile of PHPT. Methods: Clinical, biochemical, and pathological profile of PHPT presenting to a tertiary care center in South India were compared in two groups separated as per the period of presentation (Group A: January 1994–May 2007 - 51 cases and Group B: June 2007–January 2015 - 59 cases). Results: PHPT has remained a disease of female preponderance with similar age of presentation. It is being diagnosed earlier (mean duration of symptoms prior to diagnosis was 38.7 months in Group A, significantly longer than 26 months in Group B). Bone pain and metabolic myopathy were the most common presentations (60%) followed by pathological fracture (16%), renal calculi (13%), and pancreatitis (7%). Pathological fractures have become less frequent. Vit D deficiency is still a widespread co-morbidity. Radionuclide scintigraphy is an effective localizing tool, but ultrasound can be an inexpensive and widely available screening modality. Conclusion: PHPT still remains asymptomatic disease of bones and stones, although it is being diagnosed early. Greater awareness, Vit D supplementation, and better diagnostic tools have made it a disease with lesser morbidity and effective cure.

Non-hemorrhagic dengue fever with rhabdomyolysis

Acute kidney injury occurs in 33-50% of patients with rhabdomyolysis and infections remain one of the major contributing factors. The incidence of rhabdomyolysis in non-hemorrhagic dengue virus infection is quite low and may go unnoticed, especially if the presentation is not florid. We report a case of a young male patient, sero-positive for dengue, with no hemorrhagic manifestations or hypotension, who developed rhabdomyolysis complicated by renal failure. The patient eventually needed dialysis support and later recovered fully. Clinicians need to be aware of the occurrence of rhabdomyolysis even in patients without the hemorrhagic manifestations of dengue viral infection and should employ early preventive strategies in such cases.

Tackling the ‘brown’ frown

A 41-year-old non-diabetic hypertensive male with chronic kidney disease (Stage V secondary to chronic interstitial nephritis) on maintenance haemodialysis presented with a recent onset of pain in the right lower limb. An X-ray of the lower leg showed a solitary, lytic soap bubble-like mass in the lower end of the fibula (Figure 1). Labs showed a serum creatinine of 11.4 mg/dL, blood urea 124 mg/dL, Na 137 mEq/dL, K 4.5 mEq/dL, Ca 8.1 mg/dL, phosphorous 3.8 mg/dL, intact parathyroid hormone (PTH) 1688 pg/mL (normal 10–55 pg/mL), alkaline phosphatase 822 U/dL (normal 40–150 U/L) and a Vitamin D level of 65 ng/mL (normal 30–74 ng/mL). Radionuclide bone scan showed an increased uptake at the lower end of the fibula. A diagnosis of chronic kidney disease with secondary hyperparathyroidism and brown tumour of the fibula was made. He was continued on oral calcium carbonate (1 g), non-calcium-based phosphate binders (sevelamer carbonate 2400 mg), calcitriol (1 mcg thrice weekly) and cinacalcet (90 mg) with a periodic dose titration based on levels of calcium, phosphorus and PTH. After 2 years, an almost complete recovery of the brown tumour was seen (Figure 2) with a serial decreasing trend of serum PTH from 1688 to 845, 762, 512 and 190.7 pg/mL at the last visit. Brown tumours result from excess osteoclast activity and bone remodelling, which occurs in response to elevated PTH levels. They consist of a collection of osteoclasts intermixed with fibrous tissue and poorly mineralized woven bone [1], the brown coloration primarily due to haemosiderin deposition. Radiologically, they are well-defined presenting as lytic lesions with intact, thinned out and expanded cortex [2]. They are hypervascular on angiograms and intensely active on bone scans [3]. We emphasize the fact that many patients with brown tumours, who are not candidates for corrective parathyroid surgery owing to their various comorbidities, do considerably improve on medical treatment with cinacalcet circumventing complications, such as fractures, spinal cord compression, disfiguration and diplopia. This case highlights the resolution of a brown tumour with medical management via lowering of high PTH.