End-stage kidney disease patients from ethnic minorities and mortality in coronavirus disease 2019.

INTRODUCTION: Coronavirus disease 2019 (COVID-19) adversely affects patients who are older, multimorbid, and from Black, Asian or minority ethnicities (BAME). We assessed whether being from BAME is independently associated with mortality in end-stage kidney disease (ESKD) patients with COVID-19. METHODS: Prospective observational study in a single UK renal center. A study was conducted between March 10, 2020 and April 30, 2020. Demographics, socioeconomic deprivation (index of multiple deprivation), co-morbidities (Charlson comorbidity index [CCI]), and frailty data (clinical frailty score) were collected. The primary outcome was all-cause mortality. Data were censored on the 1st June 2020. FINDINGS: Overall, 191 of our 3379 ESKD patients contracted COVID-19 in the 8-week observation period; 84% hemodialysis, 5% peritoneal dialysis, and 11% kidney transplant recipients (KTR). Of these, 57% were male and 67% were from BAME groups (43% Asian, 17% Black, 2% mixed race, and 5% other). Mean CCI was 7.45 (SD 2.11) and 3.90 (SD 2.10) for dialysis patients and KTR, respectively. In our cohort, 60% of patients lived in areas classified as being in the most deprived 20% in the United Kingdom, and of these, 77% of patients were from BAME groups. The case fatality rate was 29%. Multivariable cox regression demonstrated that BAME (hazard ratio [HR]: 2.37, 95% CI: 1.22-4.61) was associated with all-cause mortality after adjustment for age, deprivation, co-morbidities, and frailty. Associations with all-cause mortality persisted in sensitivity analyses in patients from South Asian (HR: 2.52, 95% CI: 1.24-5.12) and Black (HR: 2.43, 95% CI: 1.04-5.67) ethnic backgrounds. DISCUSSION: BAME ESKD patients with COVID-19 are just over twice as likely to die compared to White patients, despite adjustment for age, deprivation, comorbidity, and frailty. This study highlights the need to develop strategies to improve BAME patient outcomes in future outbreaks of COVID-19.

Contrast Induced Nephropathy In High Risk Patients - Myth Or Reality.

BACKGROUND: Contrast induced nephropathy (CIN) is a potential stumbling block in administration of contrast media. CIN has been defined as an elevation of serum creatinine (sCr) of more than ≥0.5 mg/dl (44 µmol/l) or 25% from the baseline within 48-72 hours in the truancy of alternate tenets of acute kidney injury. Incidence of CI-AKI in patients undergoing coronary angiography with normal baseline renal function was reported to be <3%. However, the occurrence of CI-AKI was found to be as high as 50% in CKD patients undergoing Coronary Angiography. This high incidence reported by different studies is mainly because of the difference in definition, underlying renal failure, type and dose of contrast media used and frequency of other co-existing important causes of acute kidney injury (AKI). Recent studies have been published showing that risk of CIN is an overestimated and over-reckoned entity in literature. Objective: To determine the frequency of CIN in CKD patients with Creatinine clearance (Crcl) less than 60 ml/min undergoing contrast exposure. METHODS: We conducted Prospective, controlled single center trial in 42 patients having the creatinine clearance of less than 60 ml/min, they were risk stratified according to Mehran scoring system and underwent coronary angiography or contrast enhanced CT scan with contrast and specific protocol for prevention of CIN including intra-venous (IV) hydration with 0.9% Normal Saline was given before the procedure and were followed up to initial 72 hours post procedure. RESULTS: 33 out of 42 patients, i.e., got adequate hydration as per protocol however 11 patients underwent procedure as pre-existing condition did not allow so. Out of 42 patients, risk stratification according to Mehran Scoring system revealed that 15 patients out of 42 patients were included in very high risk group, 14 were in high risk group and 13 patients were in intermediate risk group. Our experience revealed that 5 out of 42 patients (11.3%) were those who experienced CI-AKI and interestingly none of them required haemodialysis. CONCLUSIONS: Our study has raised serious question on incidence of CIN in high risk patients as reported previously. However, more studies are needed over this issue till that time we might consider CIN A myth rather than a reality.

Immune thrombocytopenic purpura presenting in a patient after renal transplant for diabetic nephropathy.

BACKGROUND: Immune thrombocytopenic purpura (ITP) is primarily characterized by immune-mediated destruction of platelets in circulation. Major treatment options range from careful observation, steroids, immunosuppressive medications, immunoglobulins to splenectomy. Interestingly and rarely, ITP has also been reported after solid organ transplantation in patients receiving immunosuppressive medications. While the incidence of new onset ITP after solid organ transplant is comparatively well documented, new onset ITP after renal transplant has only been reported in two patients. Both these patients underwent renal transplant for underlying Immunoglobulin-A (IgA) nephropathy and were treated effectively with steroids. We present successful management of the first reported case of new-onset ITP presenting after renal transplant in a patient with underlying diabetic nephropathy. The case report discusses the potential management strategies in such a novel scenario aiming simultaneously for a well-functioning renal graft, adequate hemostasis, minimum therapy- related morbidity and least cost implications for the patient. CASE PRESENTATION: A 43-year-old male with hypertension and diabetes mellitus (DM), complicated by nephropathy and retinopathy, underwent pre-emptive living related renal transplant by donation from his 33-year-old wife. His immediate post-transplant period was unremarkable. Six months after the transplant, he presented with isolated thrombocytopenia. An extensive workup revealed no clinical or laboratory evidence of unusual substance intake, infection, hemolysis, microangiopathy, autoimmune disease or hematological malignancy. Eight months after the transplant, while the patient was maintained on steroids, cellcept and tacrolimus, his platelet count dipped to 13,000/microL and he had an episode of mild epistaxis. He was administered steroids in line with the adult ITP management protocol. Steroids were well tolerated, and platelet counts showed a good response to therapy. Steroids were then successfully tapered over the next ten weeks with steady and acceptable platelet counts and graft function. CONCLUSIONS: The case report discusses the diagnostic considerations and successful management of new-onset post-renal transplant ITP. It also highlights the various therapeutic options available in the medical armamentarium including shuffling of immunosuppressive drugs, rituximab, thrombopoietin receptor agonists (TPO's) and splenectomy for their potential use in complicated scenarios like relapsing, or steroid-refractory post renal transplant ITP.