FSGS diagnosis

(1) how to reduce the rate of misdiagnosis. FSGS is a morphological diagnosis of an organization, in view of the hardening of the small ball as a focal distribution, found only in early disease nearly medullary renal unit, it is easy to misdiagnosis. In recent years, scholars have stressed the need for a sufficient number of biopsy specimens, and stressed that found a segmental sclerosis of glomerular enough to be diagnosed as of FSGS. According to probability estimates, 10 glomerular specimens missing rate of 35%, 20 glomerular enable the missed rate dropped to 12%. Authors suggest that, if the credibility of the FSGS diagnosis 95%, 99%, 99.5%, the minimum number of glomerular consecutive imprints on each cross-section need be for 7,8,9, but the slice cross sectiondistance of less than 27μm or 23μm [8]. Material restrictions not found in the glomerular segmental sclerosis, following 3:00 prompt FSGS have a certain reference value, namely (1) abnormalities of glomerular hypertrophy. A pediatric small lesions that later develop into FSGS the glomeruli than their peers in the control group and re-biopsy is still minimal change glomerular increased significantly. (2) with minimal change in the foot process fusion completely compared to that of FSGS foot process fusion is incomplete. (3) of FSGS is often accompanied by varying degrees of renal tubular damage, so check to see the small tube of focal atrophy with interstitial change is also a valuable reference.
Two different parts of the glomerular sclerosis. In recent years, noted that FSGS sclerosis lesions have a different distribution in the glomerulus, and its primary disease due and prognosis. Common change of five kinds: (1) hardening occurs in the glomerular urinary pole. (2) glomerular sclerosis occurs in blood vessels with a very transparent degeneration. (3) glomerular sclerosis in the capillary loop margin with parietal epithelial cell adhesion. (4) collapse of glomerular sclerosis. (5), diabetic nephropathy unique to tuberous sclerosis and hyalinization of the capillary arteries. Due to the cause, the variety of pathophysiological mechanisms of glomerulosclerosis area can see Schiff acid-positive cell-free material, but its composition may be different. In the glomerular vascular pole most of the renal atrophy and poor prognosis; located in the urinary pole, the so-called cutting-edge lesions, suggesting that the early lesions, the prognosis is good. The margin of lesions are most common in the pediatric, mixed lesions and vascular pole lesions is more pronounced in adults, but all the hardened forms can be found in all age groups. The morphological characteristics of illness thus different. Secondary to reflux nephropathy, often around the renal capsule fibrosis and Bowman's capsule, interstitial thickening and spotty scarring. Heroin kidney epithelial cells change, the onset of interstitial fibrosis and tubule damage bit more obvious. The human immunodeficiency virus (HIV) infection caused by focal scarring, severe renal damage, including cystic dilatation, as well as glomerular vascular atrophy and electron microscopy to see the network organization gathered on the endothelial cells.
3. Except of systemic disease or primary renal disease secondary of FSGS. : Confirm the primary or idiopathic FSGS, except a variety of secondary glomerular hypertrophy / hyperfiltration due to of FSGS (such as solitary kidney, reflux nephropathy, unilateral renal resection, a variety of reduced nephron caused by kidney disease, diabetes, hypertension, obesity, sickle cell disease, etc.) and due to renal scarring cause of FSGS (such as IgA nephropathy, polyarteritis, lupus nephritis, hereditary nephropathy, etc.). In addition, the need to except the human immunodeficiency virus infection and heroin, cocaine addict kidney changes.
Commonly used clinical indicators in glomerular diseases FSGS diagnosis and its severity predicted value. Of FSGS clinical: 97% had proteinuria, microscopic hematuria 91%, hyperlipidemia 83%, 68% of the urinary tube, hypertension 67%, 50% of nephrotic syndrome, renal dysfunction, 47%, family history of 11 %.
Due to the trauma of the kidney biopsy, kidney disease scientist trying to explore some of the features associated with the indicators to be diagnosed and prognosis. (1) urinary protein often clues of FSGS, but neither diagnosis is difficult to estimate the extent of of FSGS. Proteinuria is mainly caused by the non-hardening of the permeability of the glomerular capillary wall abnormalities, no direct correlation with FSGS. And extensive glomerular sclerosis, proteinuria but started to decrease. Furthermore proteinuria and glomerular capillary hemodynamic abnormalities. Therefore, to improve the hemodynamic drugs such as angiotensin converting enzyme inhibitors, although in the short term to reduce urinary protein but does not affect the morphology. (2) serum creatinine is also commonly used clinical indicators, FSGS can uniquely affect the glomerular filtration function activated, and some lesions of glomerular function decreased by other alive glomerular function enhanced to compensate, so the FSGSdegree and creatinine levels can be very different. (3) changes in glomerular filtration rate (GFR): FSGS is usually accompanied by a small tube between the different levels of quality change, the lack of the integrity of the tubule, GFR markers, such as creatinine, can reflux back into the blood circulation, rather than from the urine, leading to underestimate the level of GFR. And renal blood flow change can also affect the GFR.Some antihypertensive drugs (angiotensin converting enzyme inhibitors), effectively reduce glomerular capillary pressure, which led to the decline in GFR. Such a drastic decline in GFR is not caused due to deterioration in FSGS organizations learn.
To sum up, this feature of FSGS - the reason for the discrepancy in the structure can be summarized as: (1) focal segmental distribution of lesions; (2) loss of renal units; (3) of the complete glomerular compensatory ; (4) renal blood flow change; (5) plasma osmotic pressure changes and changes in glomerular local pressure; (6) tubulointerstitial changes.