TB, DM, and renal impairment

The WHO recommends LTBI screening for dialysis patients and CKD stage 3+ due to elevated TB risk from immune deficiencies in ESRD. Risk factors include hyperparathyroidism, malnutrition, oxidative stress, vitamin D deficiency, and gender bias. CKD causes immune dysfunction via apoptosis, lymphocyte loss, PMNL issues, and uremic toxins. Dialysis worsens this by depleting essential nutrients or causing immune reactions from membrane incompatibility or contamination. TB symptoms like anorexia and fatigue mimic those of renal failure. Extrapulmonary TB most commonly affects lymph nodes, then pleural, peritoneal, and urinary systems. The IGRA test (QFT-GIT) using ESAT-6/CFP-10 proteins better differentiates true infection from BCG or non-MTB cross-reactions. IGRA is useful for studying immunocompromised patients, and treating LTBI with a 3-month regimen of weekly rifapentine and isoniazid (3HP) is key to TB control in this group.[1]

The convergence of diabetes and TB epidemics is particularly pronounced in South-East Asia, the Western Pacific, and the Middle East, driven by rising diabetes due to obesity and aging populations. Diabetes worsens TB outcomes by increasing mortality, treatment failure, and relapse rates. It impairs immune response by reducing antigen presentation and interferon-γ production, crucial for TB control. TB itself can lead to insulin resistance, potentially causing 'stress-induced hyperglycaemia' and increasing T2D risk. Diabetes management affects microvascular complications like diabetic kidney disease, which, in CKD patients, leads to immune compromise and increased hospitalization and mortality risks related to eGFR decline.[2]

In New Zealand, diabetic nephropathy is a major cause of CKD, with significant implications for dialysis. However, assessing the relationship between diabetes and renal failure is complex due to HbA1c's unreliability in reflecting long-term glucose control in patients with haemodialysis, anemia, or on erythropoietin. Early CKD might show hyperglycaemia, but as renal function deteriorates, insulin clearance decreases, leading to seemingly better glycaemic control which can mask previous poor control responsible for renal damage, thus complicating the interpretation of hospitalization and eGFR data.[2]

References:

1. Zhang, X., Chen, P. and Xu, G., 2022. Update of the mechanism and characteristics of tuberculosis in chronic kidney disease. Wiener klinische Wochenschrift, 134(13), pp.501-510.

2. 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.