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  1. Suleman AA, Abd Ghani F, Fadhlina NZ, Rafidah H
    Med J Malaysia, 2024 Jan;79(1):95-101.
    PMID: 38287764
    INTRODUCTION: Immunoglobulin A (IgA) nephropathy (IgAN) results from abnormal accumulation of immune complexes containing galactose deficient IgA1 (Gd-IgA1) in the kidneys. About 40% of patients develop end-stage kidney disease within 20 years of renal biopsy. At present, the diagnosis and risk stratification of patients (using the international IgAN risk prediction tool) rely on renal biopsy, which is an invasive procedure. Also, treatment decisions are still dependent on proteinuria, which is not specific for IgA nephropathy. We discussed the role of serum and urine Gd- IgA1 in the diagnosis of IgAN, its association with disease progression and changes with treatment in patients with IgA nephropathy.

    MATERIALS AND METHODS: A systematic search of PubMed and Scopus databases was done to identify the articles that are relevant to the topic including systematic reviews and original articles.

    RESULTS: Several studies showed that both serum and urine Gd-IgA1 differentiate IgA nephropathy patients from healthy people and other glomerulonephropathies. Thus, it is useful as a less invasive diagnostic biomarker, although detection methods varied between studies with different sensitivities. There are various reports of its use as a prognostic parameter. Evidence is emerging for its use as a monitoring parameter for treatment.

    CONCLUSION: Galactose deficient IgA1 is a promising biomarker in the management of IgA nephropathy, although a more robust and standardised means of estimation is required.

  2. Lim CTS, Nordin NZ, Fadhlina NZ, Anim MS, Kalaiselvam T, Haikal WZ, et al.
    BMC Nephrol, 2019 01 16;20(1):22.
    PMID: 30651084 DOI: 10.1186/s12882-019-1203-7
    BACKGROUND: Although there is a large volume of literature regarding the definition and epidemiology of. Type 2 diabetes nephropathy (T2DN). There has been a paucity of data focused on the rate of transition of T2 DN. Based on our personal observation a certain percentage of our incident end stage renal disease (ESRD) patients from T2DN experienced a rapid decline of renal function. Their rapid decline nature of glomerular filtration rate (GFR) of 46 to 60 mL/min per 1.73m2 per year have far exceeded the KDIGO definitions of acute kidney injury (abrupt decrease in kidney function occurring over 7 days or less), acute kidney disease (acute or subacute damage and/or loss of kidney function for a duration of between 7 and 90 days after exposure to an acute kidney injury initiating event (Chawla et al Nat Rev Nephrol 241-57 2017) or even rapid decliner (eGFR declines > 5 mL/min per 1.73m2 per year) (Chawla et al Nat Rev Nephrol 241-57 2017; Andrassy Kidney Int 622-623 2013).

    CASE PRESENTATION: We describe here three cases of type 2 diabetic patients that have rapid renal deterioration with rate of decline 46 - 60 mL/min per 1.73m2 per year. All the patients are heavily nephrotic. All of the renal biopsies done showed the classical diabetic changes, hypertensive changes, diffuse tubulointerstitial damage, and interstitial nephritis. All of the patients admitted to taking various form of traditional medications in hope of curing their renal disease.

    CONCLUSION: We wish to highlight that type 2 diabetics with massive nephrotic range proteinuria have enhanced risk of rapid renal function deterioration. The patients should be educated about the risks of rapid renal function deterioration when there is presence of heavy proteinuria. High grade proteinuria is likely to inflict the diffuse tubulointerstitial inflammation. The interstitial nephritis could be further worsened by traditional supplements consumption. Timely health education and advice must be undertaken to retard this unwanted rapid renal disease progression.

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