Chronic Glomerulonephritis

An overview of chronic glomerulonephritis (GN chronic) means all Causes of different pathological types of glomerular bilateral diffuse or focal inflammation, clinical onset hiding, long duration, disease develops slowly over a group of primary glomerular diseases known, it is not strictly speaking an independence of the disease. But not because of clinical extensive kidney biopsy. This group of chronic glomerulonephritis clinical syndrome - clinical work on the development of treatment and prevention programs and renal disease progress deterioration can be useful, it still retains chronic glomerulonephritis one. Etiology of chronic nephritis is a group of more than glomerular etiology of chronic disease mainly of glomerular disease, but most patients with unknown etiology. with streptococcal infection is not clear, according to statistics only 15% ~ 20% from acute glomerulonephritis to change, But due to acute glomerulonephritis Asia clinical diagnosis is not easy, so the percentage actually may be higher. In addition, the majority of patients with chronic nephritis acute nephritis history, Therefore, more scholars believe that the current chronic glomerulonephritis and acute nephritis have no definite correlation, It may be due to bacteria, viruses or parasites and other infections through immune mechanisms, inflammatory mediators factor and non-immune mechanism caused the disease. Pathological changes of chronic glomerulonephritis pathological changes and their causes, course and type different. Can be in the form of diffuse or focal segmental glomerular mesangial proliferative, proliferative membranes, membrane, small lesions, focal glomerulosclerosis, glomerular advanced fibrosis or not stereotypes. In addition to glomerular disease, but will also associated with varying degrees of renal interstitial inflammation and fibrosis, renal interstitial damage increased renal dysfunction. Glomerulonephritis advanced renal cortical thinning and shrinking of glomerular capillary loops development of the glass-like change or fibrosis, residual glomerular can compensatory increases, tubular atrophy, and so on. Typical cases the diagnosis is not difficult to diagnose, with proteinuria, hematuria (phase contrast microscopy was mostly in the number of red blood cells to change shape), hypertension, edema, renal dysfunction glomerulonephritis, and other clinical manifestations, course lasted for more than a year, except secondary glomerulonephritis caused, and we should consider this disease. In the differential diagnosis of chronic need pyelonephritis with chronic renal interstitial nephritis, lupus nephritis, Purpura Nephritis and hereditary nephritis and other equivalent identification. Most of the clinical performance of misprision of onset, long duration, disease progress more slowly. As different types of pathology, clinical performance inconsistencies, the majority of cases are headed to edema symptoms, uneven. Only mild facial and leg-swelling, severe nephrotic syndrome may arise, Some cases of hypertension was headed by the symptoms are found to chronic glomerulonephritis. Performance can be asymptomatic proteinuria and / or hematuria. Or just emerging polyuria and nocturia. Throughout the course of disease or no obvious physical decline until the emergence of severe anemia or uremia for the first symptom, generally different clinical manifestations, is divided into the following five subtypes : (1) common type is more common. Chronic disease, the condition is relatively stable, more performance for mild to moderate edema, hypertension and renal dysfunction. (+)~(+++), Centrifugal urinary protein in urine RBC "10 / HPF and other urinary tube. Pathological changes in mesangial proliferative focal segmental glomerular mesangial proliferative and mesangial proliferative glomerulonephritis seen more often. (2) Except nephropathy-the-ordinary performance, mainly for nephrotic syndrome, 24-hour urine protein "3.5g, serum albumin less than 30 g / L, generally heavier and edema associated with or without hyperlipidemia. Pathological type lesions in small, membrane, the membrane proliferation, focal glomerulosclerosis as the styles. (3) In addition to the above-hypertension - ordinary performance, continuing to moderate high blood pressure as the main performance, especially sustained increases in diastolic blood pressure, accompanied retinopathy artery thin, twisting and arteries and veins cross oppression, Minorities have floc exudation and / or bleeding. Pathology focal segmental glomerular sclerosis and diffuse proliferation of styles or late or not a stereotypical performance glomerulosclerosis. (4) mixed in both clinical nephropathy-type performance with the performance of hypertension, Meanwhile more with different degree of renal dysfunction signs. Pathological changes to the focal segmental glomerular sclerosis and advanced diffuse proliferative glomerulonephritis, and so on. (5) acute type in relatively stable condition or course of continued progress, Because bacteria or virus infection or fatigue, and other factors, the shorter the incubation period (for a more ~ 5), and acute nephritis similar clinical manifestations, treatment and rest restore stability to the original level or got worse, uremic gradually occurred; Recurrent or repeatedly, dramatically reduced renal function uremic there is a series of clinical performance. Pathological changes to diffuse proliferation, glomerular sclerosis on the basis of emerging or crescent and obvious interstitial nephritis. Chronic glomerulonephritis clinical and pathological pattern is not absolute, various types can be transformed into each other between, right kidney biopsy failed to make pathological type of the disease that can be the basis of clinical features make nephritis, nephrotic syndrome, hypertension, the sub-type; Determination of renal function, as a rough estimate severity, the development of treatment programs and determine the prognosis of reference. A few patients with chronic nephritis clinical manifestations has been alleviated or not obvious, but the pathological changes and the end of restoration, or even more serious development, in an acute attack after uremia. Therefore, emphasis should be closely observed and the importance of follow-up. Azotemia chronic nephritis [it] refers to the etiology and pathology of various types of primary glomerular disease, in the development of diseases that occur during light to moderate damage glomerular filtration function, the performance of urea nitrogen and serum creatinine increased, endogenous creatinine clearance rates were lowered, In fact, azotemia appeared at the same time or before have varying degrees of renal function. Azotemia chronic nephritis is the development of chronic renal failure as a prelude, but in the interim, light young patients often feel good about themselves, lightly, and the other part of the course regardless of the length of nephritis. azotemia also emerged that it is often mistaken for the development of the disease is the natural outcome of uremia phenomenon. According to the clinical observation that many patients with chronic nephritis azotemia by a stage renal function after treatment can be markedly improved, in a very long period of time could maintain good kidney function and the presence of reversible factors, and the other part in a relatively short period of a few years or for the progress of uremia. China accounted for chronic nephritis uremia Etiology first, it should pay attention to the clinical study of chronic nephritis azotemia pathological basis. Pathophysiology, as well as other factors reversible factors, in order to adopt targeted prevention measures, reversible in some patients for more effective solutions to chronic renal failure occurred and development. In the diagnosis and treatment should be noted. 1. Azotemia and clinical assessment should first understand the extent of renal before any drugs on the factors and the impact of creatinine clearance. Patients with normal renal function occurred mild cardiac output or blood volume reduction shortage of glomerular filtration rate and little impact on chronic nephritis azotemia patients the same degree of cardiac output or blood volume change, can often significantly higher azotemia, even multiplied. Some commonly used drugs can cause false serum creatinine, such as cimetidine, and the long-term SD-dopa, cefoxitin and ketone body, and so on. Dynamic Assessment of glomerular filtration rate can understand kidney disease severity. Commonly used method for determination of serum creatinine, creatinine clearance and blood urea nitrogen, Scr and Ccr have some relevance, generally Scr1lmg/dl, Ccr to 100ml/min; dependent equivalent Ccr50ml/min, 4mg/dl equivalent to 25ml/min, azotemia so often to the extent of 2.5 0.8IU/ml Scr below Ccr in 40ml/min more mild; Scr "2.5mg/dl, Ccr "40ml/min moderate, and ≥ 3.5mg/dl of serious Scr. BUN of many factors, but sometimes in acute renal injury, and did not change Scr BUN increased significantly. Scr can also be used in the formula to reflect Ccr, it is simple and practical and can be used as a rough estimate of reference. Ccr (ml / min) = (140-age) x weight (kg) / 72 × serum creatinine (mg / dl ) 2. to seek short-term sexual emerged or emerging azotemia azotemia the influencing factors in patients with chronic nephritis Man long course of a few years China has slowly increased Scr is often the development of the disease process. But many patients originally renal function or long-term stability in the investigation of renal function, in an infection or fatigue or there, severe hypertension of pregnancy or after childbirth or after the application of certain drugs after Scr increased significantly, This often part of cases of acute or temporary factors and not mistaken for chronic nephritis uremia Renal sometimes light microscope can still see glomerular mesangial cell proliferation obviously, glomerular score. Ball out a small artery fibrinoid necrosis, even small cystic renal cell with crescent formation and / or renal interstitial inflammatory cells to severe infiltration, Most of these cases were good general condition, can tolerate hormone therapy, After 80 ~ 240 mg of methylprednisolone infusion 5 ~ 10 days or prednisone to 40 ~ 60 mg / 2 ~ 4 days Zhou, renal function improved in varying degrees often, even Scr back to normal. Hence, the performance for various types of patients with chronic nephritis first appears significantly higher Scr should be carefully looking for reversible factors, right nephrotic syndrome membranous nephritis, mesangial proliferative diseases such as hypercoagulable state associated with the patients still should be excluded from renal vein thrombosis. caused or exacerbated azotemia. Renal CT scan can often found renal vein thrombosis.