TB and DM: increased hospitalisations and mortality associated with renal impairment

Kaur, R., Egli, T., Paynter, J., Murphy, R., Perumal, L., Lee, A., Harrison, A., Christmas, T., Lewis, C. and Nisbet, M., 2023. Tuberculosis and diabetes: increased hospitalisations and mortality associated with renal impairment. Internal Medicine Journal, 53(9), pp.1588-1594.

  • Geographical Impact:

    • The merging of diabetes and TB epidemics is most notable in South-East Asia, the Western Pacific, and the Middle East, where diabetes is also highly prevalent.
    • While global TB rates are declining, diabetes prevalence is increasing due to obesity and an ageing population.

  • Diabetes and TB Interactions:

    • In TB patients, diabetes increases the risk of mortality, treatment failure, and TB relapse.
    • High glucose conditions reduce phagocyte antigen presentation to T-helper cells, decreasing interferon-γ production, which is necessary for macrophages to kill TB.
    • Active TB induces insulin resistance through the production of ‘stress’ hormones and cytokines (IL-1, TNF-alpha, and IL-6), causing impaired glucose tolerance (IGT) in non-diabetic individuals.
    • ‘Stress-induced hyperglycaemia’ resolves with adequate TB treatment but may signal underlying pancreatic beta-cell insufficiency, increasing the long-term risk of developing type 2 diabetes (T2D).

  • Impact on Microvascular Complications:

    • Prolonged inadequate diabetes control increases the risk of microvascular complications, including diabetic kidney disease.
    • Chronic kidney disease (CKD) patients experience compromised immunity, reducing both innate and adaptive immune responses.
    • In these patients, the odds of hospitalization increase by 2% with every unit decrease in eGFR (measured in mL/min/1.73 m²), and mortality odds increase by 6% with every year of age and by 3% with every unit decrease in eGFR.

  • New Zealand Context:

    • In New Zealand, diabetic nephropathy is the leading cause of chronic kidney disease, with diabetic kidney disease accounting for about half of all dialysis patients.
    • Assessing the correlation between renal failure and diabetes is challenging when comparing current eGFR with current HbA1c, as HbA1c is not a reliable marker of cumulative hyperglycaemia burden at a single time point.
    • HbA1c reliability decreases in patients on haemodialysis, with co-existing anaemia, or on erythropoietin-stimulating agents.
    • Early CKD may present with relative hyperglycaemia, but as renal failure progresses, apparent glycaemic control improves due to reduced insulin clearance, reduced renal gluconeogenesis, and poor appetite/malnutrition.
    • Consequently, HbA1c may appear low, masking past poor diabetes control that drove renal failure, complicating the understanding of the relationship between hospitalization and eGFR. 

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