Nephropathology in SLE which is not part of the classic lupus nephritis
What nephropathology occurs in patients with SLE that is not part of the classic lupus nephritis?
Although glomerular inflammatory involvement is the prototypical example of lupus nephritis, the tubules, interstitium, and vasculature of the kidney can also be affected.
• Tubulointerstitial disease: proximal tubular dysfunction and hyperkalemic renal tubular acidosis can be seen in patients with lupus. Acute interstitial nephritis including active tubulitis (infiltration and invasion of the tubules) can be seen with or without glomerular disease.
• Podocytopathy: the epithelial cells in the glomerular capillaries may become effaced, termed podocytopathy , which typically gives rise to the dramatic onset of the nephrotic syndrome, similar to the clinical presentation of minimal change disease.
• Antiphospholipid syndrome (APS): antiphospholipid antibodies (aPL) can be seen in up to 40% of SLE patients, and about 50% of these patients can develop APS. APS is characterized by a combination of arterial and/or venous thrombosis in the setting of positive aPL. Thus patients are at risk for renal artery stenosis and thrombosis, renal vein thrombosis, and renal infarction. Antiphospholipid nephropathy (APSN) refers to the vascular lesions in glomeruli, small arteries, arterioles, and interlobular arteries seen in patients with persistent aPL (with or without APS). TMA is the distinct histologic finding in acute lesions. Chronic vascular lesions include arterial fibrous intimal hyperplasia, arteriosclerosis, and organized thromboses. Kidney manifestations of APS can occur in the presence or absence of lupus nephritis, and APSN can be associated with all classes of lupus nephritis.
• Acute tubular necrosis and interstitial nephritis can be seen in patients taking nonsteroidal anti-inflammatory agents for arthritis.
