Onset and clinical manifestations of IgA nephropathy

  IgA nephropathy is a glomerulonephritis characterized by IgA deposition in the glomerular thylakoid region. IgA nephropathy is divided into two categories: primary and secondary. IgA nephropathy is a progressive disease, and only 5%-30% of patients with IgA nephropathy have complete remission of urinalysis abnormalities; most patients have chronic progressive development. IgA nephropathy is the leading cause of end-stage renal disease in China, and the risk factors for progression of IgA nephropathy are glomerulosclerosis, interstitial fibrosis, hypertension, massive proteinuria and renal hypofunction.  The etiology of primary IgA nephropathy is not fully understood. Common etiologies of secondary IgA nephropathy include allergic purpura, viral hepatitis, cirrhosis, systemic lupus erythematosus, ankylosing spondylitis, rheumatoid arthritis, mixed connective tissue disease, polyarteritis nodosa, erythema nodosum, psoriasis, ulcerative colitis, Crohn’s disease, tumors, and AIDS.  IgA nephropathy can manifest clinically as isolated hematuria, recurrent episodes of sarcoid hematuria, asymptomatic hematuria and proteinuria, and can also be combined with edema, hypertension, and hyperalgesia, manifesting as nephritis syndrome or nephrotic syndrome.  Recurrent episodes of granulomatous hematuria, mostly appearing hours or days after mucosal or cutaneous infection, reduce or disappear after infection control. During the period of sarcoid hematuria, most of them have no obvious conscious symptoms, and occasionally there is a feeling of back pain and swelling. The course of the disease is often self-limiting, and most patients have a good prognosis, and renal function can remain stable for a long time.  Asymptomatic urinalysis abnormalities include simple asymptomatic microscopic hematuria and persistent microscopic hematuria with mild to moderate proteinuria (proteinuria less than 3.5g/24h). Most patients have an insidious onset, and most of them have no clinical manifestations such as hypertension and renal insufficiency at the time of onset. In some patients, the disease may progress and hyperalgesia may occur.  IgA nephropathy can also be characterized by persistent proteinuria (urine protein greater than or equal to 3.5g/24h) or even nephrotic syndrome. If IgA nephropathy with massive proteinuria is combined with significant hematuria, hypertension and renal hypofunction, the disease is likely to progress. If the renal function deteriorates rapidly, combined with significant hematuria and large amount of proteinuria, cellular crescent formation and capillary collaterals necrosis should be considered, and renal biopsy should be performed as soon as possible to clarify the diagnosis.  Hypertension is one of the common clinical manifestations of IgA nephropathy. At the time of definitive diagnosis of IgA nephropathy by renal biopsy, about 40% of patients have hypertension. The incidence of hypertension increases with the prolongation and aggravation of the disease. Patients with combined hypertension may have varying degrees of hematuria, proteinuria and renal insufficiency as well as hyperuricemia. A small number of patients present with malignant hypertension and rapid progressive deterioration of renal function.  In addition to proteinuria, microscopic hematuria and hypertension, other manifestations of chronic renal insufficiency, such as anemia, nocturia, etc., are also present in some patients. Many patients have lost the opportunity of kidney biopsy.  Urinary red blood cells in IgA nephropathy are mostly aberrant red blood cells, especially the presence of odontoclasts or spiny red blood cells, which are of greater value for diagnosis. However, the proportion of normal red blood cells in the urine may increase when hematuria is evident in the naked eye. Urine protein quantification is more common in small to medium amounts and is non-selective proteinuria. Serum IgA is increased in some patients. In patients with renal insufficiency, blood creatinine, urea nitrogen and blood uric acid are increased. Even in patients with IgA nephropathy with normal renal function, some of them have elevated blood uric acid.