Incidence of needlestick injury among healthcare workers in western India.

BACKGROUND OBJECTIVES: Injuries occurring from contaminated sharps are a major occupational health hazard. It carries a risk of transmitting blood-borne diseases such as human immunodeficiency virus (HIV), hepatitis B and hepatitis C. Healthcare workers (HCWs), including personnel handling biomedical waste, are at risk. The objective of this study was to determine the incidence and details of needlestick injury (NSI) among HCWs. METHODS: We analyzed data of all HCWs who reported NSI over the past three years. Demographic details, type and source of injury, use of personal protective equipment (PPE), immediate post-exposure measures, hepatitis B vaccination status and HCWs and source's HIV, hepatitis B and hepatitis C serological status were studied. RESULTS: Fifty-six cases of NSI were recorded over three years, accounting for an incidence of 10.4/100 occupied beds per year. Maximum cases (73.2%) occurred between the 20 and 40 yr age group. The distribution among the work category was doctors (37.5%), nursing staff (26.8%), phlebotomy technicians (12.5%), housekeeping/subordinate staff (12.5%) and others (10.7%). Appropriate PPE was donned by 66 per cent of the HCWs. The majority of cases (46.4%) occurred in wards and operating rooms (23.2%). Phlebotomy (35.7%), followed by procedures, such as hemoglucotest (HGT) measurement, intravenous cannula insertion and operative procedures (33.9%), were the most common situation during which HCWs suffered NSI. While 64.2 per cent HCWs were vaccinated for hepatitis B, only 5.4 per cent of the HCWs completed post-exposure anti-retroviral regimen. INTERPRETATION CONCLUSIONS: We conclude that a relative lack of awareness towards preventive measures and inexperience among HCWs may be contributory to high occurrence of NSI events. This study emphasizes upon ensuring active hospital-wide hepatitis B vaccination of all HCWs and supportive therapy to improve compliance towards post-exposure prophylaxis.

Acute interstitial nephritis following SARS-CoV-2 virus vaccination.

A number of reports have described new onset or relapse of existing glomerular disease after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination. More and more of these cases continue to emerge, and the European Medicines Agency (EMA) has recently launched an in-depth investigation to ascertain the true frequency of such renal side effects. In comparison, acute interstitial nephritis after SARS-CoV-2 vaccination has only been described in 1 solitary case. Here, we describe a case of acute kidney injury due to biopsy-proven acute interstitial nephritis soon after SARS-CoV-2 vaccination with the Astra-Zeneca vaccine. The patient responded well to steroids, although he required temporary renal replacement therapy. A thorough medical history failed to elucidate any plausible explanation or trigger other than the preceding vaccination. We acknowledge the possibility that other factors could have triggered acute interstitial nephritis in the case described here. Similar uncertainty exists regarding glomerular disease reported in conjunction with SARS-CoV-2 vaccination. However, we note that acute interstitial nephritis associated with vaccination has been described before the pandemic, and we therefore feel that a link is possible. We suggest that nephrologists should be vigilant when they see cases of unexplained acute interstitial nephritis. A history of preceding SARS-CoV-2 vaccination should be explored, and cases should be reported within national systems of pharmacovigilance.

Human leucocyte antigen-associated anti-glomerular basement membrane disease in siblings.

We report a case of anti-glomerular basement membrane (GBM) disease in association with human leucocyte antigen (HLA) DRB1 15:01. A 71-year-old woman presented with oligoanuric acute kidney injury accompanied by high titre anti-GBM antibodies. Renal biopsy revealed a severe crescentic glomerulonephritis. Her brother had presented 6 years earlier with oligoanuric acute kidney injury. He was dual positive for MPO ANCA and anti-GBM antibodies. Renal biopsy was not performed. Both had an absence of pulmonary involvement. Tissue typing confirmed both were heterozygous for HLA DRB1 15:01 and DRB1 04:03.

Recurrence of Tubulointerstitial Nephritis Without Uveitis, in a Patient with Previous Tubulointerstitial Nephritis and Uveitis Syndrome After Transplant.

We report a case of recurrent tubulointerstitial nephritis without uveitis in a patient with previous tubulointerstitial nephritis and uveitis syndrome after transplant. A 26-year-old male patient who had been diagnosed with tubulointerstitial nephritis and uveitis syndrome at 8 years of age developed end-stage renal failure and subsequently underwent living-donor related renal transplant at 17 years old. The 1st recurrence of tubulointerstitial nephritis and uveitis occurred 36 months after transplant, which was treated with increased immunosuppressive drugs. Graft function worsened again to estimated glomerular filtration rate of 25 mL/min/1.73 m² at 76 months after transplant. Transplant ultrasonography was unremarkable. Virology tests (including cytomegalovirus, BK virus, and Epstein-Barr virus tests) were all negative, with negative donor-specific antibodies. Urine protein creatinine ratio was unremarkable. A biopsy showed chronic allograft rejection and graft sclerosis, and immunosuppressive medications were subsequently decreased. The patient's renal function continued to decline over the next 3 months, with estimated glomerular filtration rate showing 18 mL/min/1.73 m², prompting a further renal biopsy that showed granulomatous interstitial nephritis and moderate interstitial fibrosis. This was consistent with a further relapse of tubulointerstitial nephritis but without uveitis. His renal function improved over the next few months after tacrolimus was reintroduced.

Orlistat-induced oxalate nephropathy: an under-recognised cause of chronic kidney disease.

Two patients developed kidney failure due to oxalate deposition in the kidney while taking orlistat. Cessation of orlistat was followed by partial recovery of kidney function. The mechanism by which orlistat causes hyperoxaluria and the management of orlistat-induced oxalate nephropathy is reviewed. We suggest that all patients taking orlistat are at risk of this condition, which may develop insidiously and is easily overlooked. Monitoring of kidney function of patients taking orlistat is warranted.