Immune mediated injuries comprise a major bulk of renal disorders that mostly manifest as acute or chronic glomerulonephritides. Besides initial investigations for renal disorders, diagnosis of immune mediated renal diseases requires a battery of immunological tests and renal histopathology. The laboratory tests include anti-nuclear antibodies (ANA) followed by

• anti-double stranded deoxyribonucleic acid antibodies (antidsDNA)
• and/or anti-extractable nuclear antigens (anti-ENA),
• complement levels (C3, C4, factor H),
• rheumatoid factor (RF),
• C reactive proteins (CRP),
• anti-streptococcal antibodies including anti streptolysin-O titer (ASOT)
• and anti-deoxyribonuclease B (anti-DNAse B),
• anti-neutrophilcytoplasmic antibodies (ANCA), anti-glomerular-basement membrane antibodies (anti-GBM), cryoglobulins detection, anti-phospholipid antibodies, nephritic factor, anti-phospholipase A2 receptor antibodies (anti-PLA2R) etc.

The correct interpretation of these tests by an immunologist in collaboration with histopathologists and nephrologists is the key to an accurate diagnosis and successful management of patients with renal diseases.

Customarily renal injury or failure are broadly classified as pre-renal (azotemia), post-renal (obstructive) and interstitial renal (vascular, parenchymal or tubular) diseases. Depending on the clinical course and development of renal dysfunction, renal disorders are also categorized as acute and chronic diseases.

Baseline investigations in any kind of renal disorder include complete blood picture, detailed urine report with or without culture and sensitivity, serum creatinine, glomerular filtration rate (GFR) and creatinine clearance, 24 h urinary protein excretion, fraction excretion of sodium and albumin, cystatin C and radiological investigations such as ultrasound, computed tomography scanning etc.

Most of the renal diseases result due to immune mediated injury mainly manifesting as glomerulonephritides (GN). GN can be primary or it may be a part of other autoimmune disorders such as systemic lupus erythematosus (SLE) with multiple organ involvement or vasculitis. Immunopathogenesis of GN involves activation of complement cascades and coagulation pathways, recruitment of inflammatory cells and release of proinflammatory cytokines. Other important mechanisms include failure of apoptosis and intraglomerular hemodynamic changes. Progression to fibrosis and scarring depends upon the rate of antigen clearance or their persistence.odds ratio of 2.6 for CKD if metabolic syndrome was present.

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