Renal medicine

How accurate is glycated haemoglobin in patients with liver cirrhosis? A case series (2018)

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Type of publication:
Conference abstract

Author(s):
*Basavaraju N.; *Rangan S.; *Singh P.; *Moulik P

Citation:
Diabetic Medicine; Mar 2018; vol. 35 ; S1

Abstract:
Introduction: Glycated haemoglobin (HbA1c) is the gold standard for monitoring glycaemic control in patients with diabetes. We present three cases of chronic liver disease where HbA1c may be misleading. Case 1: A 71-year-old Caucasian woman with liver cirrhosis due to hepatitis C, Type 2 diabetes, previous bladder tuberculosis and chronic kidney disease stage 3 was evaluated in clinic. Her capillary glucose (CG) was 6 to 9 mmol/l, no hypoglycaemia. She was anaemic; HbA1c was low at 34mmol/mol. Fructosamine was elevated at 296umol/l (205 to 285). Case 2: A 38-year-old Caucasian man with alcoholic liver cirrhosis, portal hypertension, and Type 2 diabetes was admitted with haematemesis. His CG was 10 to 14 mmol/l and HbA1c 26mmol/mol. He had iron deficiency anaemia, deranged liver enzymes and renal function. Fructosamine was normal at 246umol/l. Case 3: A 65-year-old Caucasian woman with non-alcoholic steatohepatosis/cirrhosis, portal hypertension, Type 2 diabetes, iron deficiency anaemia was admitted with melena. Her CG was 12 to 14mmol/l and HbA1c 44mmol/mol. Results showed acute kidney injury, deranged liver enzymes, normal albumin but low haemoglobin. Fructosamine is awaited. All patients required insulin for management of their diabetes. Discussion: The degree of glycation (glucose binding to N-terminal valine of HbA) is dependent on glycation rate, glucose availability and lifespan of red blood cells. Reference range of HbA1c is based on normal lifespan of RBC. There are very limited studies in evaluating the accuracy of HbA1c in chronic liver disease (CLD). Multiple factors can shorten RBC survival in CLD, including anaemia, portal hypertension, hypersplenism, variceal bleeding, resulting in falsely low HbA1c. Fructosamine, glycated albumin can also be inaccurate. Capillary glucose monitoring should guide glycaemic management.

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Emerging concepts and spectrum of renal injury following Intravesical BCG for non-muscle invasive bladder cancer. (2017)

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Type of publication:
Journal article

Author(s):
*Mohammed, Azharuddin; *Arastu, Zubair

Citation:
BMC urology; Dec 2017; vol. 17 (no. 1); p. 114

Abstract:
BACKGROUNDIntravesical Bacilli Calmette-Guerin (IVBCG) therapy for non-muscle invasive bladder cancer (NMIBC) has long been in use successfully. Albeit rarely, we still face with its safety concerns more than 25 years on since its approval by US Food and Drug Agency in 1990. Local and systemic infection following intravesical BCG is widely reported as compared to immune mediated local or systemic hypersensitivity reactions involving kidneys; acute kidney injury (AKI) and other renal manifestations are well reported but not of chronic kidney disease (CKD).CASEAn interesting case of a female was referred to nephrologists in advanced stages of CKD at an eGFR of 10 ml/min/1.732 following IVBCG for NMIBC. Our patient's renal function plateaued when IVBCG was held; and worsened again when reinstilled. It introduces the concept of 'repetitive' immune mediated renal injury presenting as progressive CKD rather than AKI, as is generally reported. Although response was poor, corticosteroids stopped CKD progression to end stage renal disease.CONCLUSIONSWe highlight the need for increased awareness and early recognition of IVBCG renal complications by both urologists and nephrologists in order to prevent progressive and irreversible renal damage. Low incidence of IVBCG renal complications may also be due to under recognition in the era prior to CKD Staging and AKI Network (and AKI e-alerts) that defined AKI as a rise in serum creatinine of ≥26umol/L; hence an unmet need for urgent prospective studies. Major literature review focuses on emerging spectrum of histopathological IVBCG related renal complications and their outcomes.

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The spectrum of renal allograft failure (2016)

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Type of publication:
Journal article

Author(s):
*Chand S. , Atkinson D., Collins C., Briggs D., Ball S., Sharif A., Skordilis K., Vydianath B., Neil D., Borrows R.

Citation:
PLoS ONE, September 2016, vol./is. 11/9(no pagination)

Abstract:
Background: Causes of "true" late kidney allograft failure remain unclear as study selection bias and limited follow-up risk incomplete representation of the spectrum. Methods: We evaluated all unselected graft failures from 2008-2014 (n = 171; 0-36 years post-transplantation) by contemporaryclassification of indication biopsies "proximate" to failure, DSA assessment, clinical and biochemical data. Results: The spectrum of graft failure changed markedly depending on the timing of allograft failure. Failures within the first year were most commonly attributed to technical failure, acute rejection (with T-cell mediated rejection [TCMR] dominating antibody-mediated rejection [ABMR]). Failures beyond a year were increasingly dominated by ABMR and 'interstitial fibrosis with tubular atrophy' without rejection, infection or recurrent disease ("IFTA"). Cases of IFTA associated with inflammationin non-scarred areas (compared with no inflammation or inflammation solely within scarred regions) were more commonly associated with episodes of prior rejection, late rejection and nonadherence, pointing to an alloimmune aetiology. Nonadherence and late rejection were common in ABMR and TCMR, particularly Acute Active ABMR. Acute Active ABMR and nonadherence were associated with younger age, faster functional decline, and less hyalinosis on biopsy. Chronic and Chronic Active ABMR were more commonly associated with Class II DSA. C1q-binding DSA, detected in 33% of ABMR episodes, were associated with shortertime to graft failure. Most non-biopsied patients were DSA-negative (16/21; 76.1%). Finally, twelve losses to recurrent disease were seen (16%). Conclusion: This data from an unselected population identifies IFTA alongside ABMR as a very important cause of true late graft failure, with nonadherence-associated TCMR as a phenomenon in some patients. It highlights clinical and immunological characteristics of ABMR subgroups, and should inform clinical practice and individualised patient care.

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Are we following the guidelines to prevent contrast induced acute kidney injury? a clinical audit on patients with chronic kidney disease(CKD) undergoing coronary angiogram (2016)

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Type of publication:
Conference abstract

Author(s):
*Kanthasamy V., *Gill S.

Citation:
Global Heart, June 2016, vol./is. 11/2 SUPPL. 1(e94)

Abstract:
Introduction: Contrast induced acute kidney injury(CI-AKI) is one of the potential risk involved in high risk patients who undergo Coronary Angiography/interventions. As the procedure involved intra-arterial administration of contrast media, it expose the patient directly to the toxic side effects. It classically occurs within 72 hours of receiving the contrast media and usually recovers over the following five days. Its incidence increases significantly among the patients with risk factors and is greatly associated with short and long term mortality. The risk of CI-AKI is has been reported as high as 25% in patients with combination of CKD and diabetes, Cardiac failure, older age and exposure to nephrotoxic agents. Objectives: A clinical audit performed in order to assess the adherence to the NICE guidelines to prevent contrast induced Acute Kidney Injury among CKD patients undergoing diagnostic Coronary Angiogram and to identify the incidence of AKI following the procedure. Methods: A retrospective clinical audit was conducted to cover 6 months from May to October 2014. Data was collected from the cath lab register and patients with chronic kidney disease with eGFR<60 were included in the audit covering both in-patient and outpatient procedures(n=30). Data collection was based on the NICE guidance to look for the adherence of monitoring for renal function pre/post angiogram and considering hydration as preventive measure. Results: 93 % of the patients had two or more risk factors including CKD. All patients had renal function checked prior to the procedure but only 57 %(n=17) had post procedure renal function checked within 1 week and only 53 % were hydrated. 10 out of 17 patients( 59%) showed a decline in renal function. Among them 4 (23%) patients had AKI as per KDIGO criteria (Kidney Disease: Improving Global Outcomes) and of which 3 (75%) were not hydrated pre/post procedure. Renal function did not return to baseline in one of those 4 patients. Conclusion: In overall it was clearly evident that taking preventive measures against CIAKI in CKD patients were overlooked. Our recommendations were to introduce a checklist pre & post procedure for all patients so that high risk patients can be identified, to instruct the GP(on discharge) to re-check the renal functions in 3 days and to re-audit.