How to differentiate between native kidney proteinuria from transplant kidney proteinuria?
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Proteinuria is very common non-specific sign of the renal allograft injury. In kidney transplant recipients, the prevalence of proteinuria varies substantially and ranges between 11% and 45%. It depends on criteria for proteinuria definition and partly on the time passed after the transplant procedure. Majority of the authors investigated proteinuria 1 year after kidney transplantation. In studies with a diagnosis of proteinuria as a high content of protein (exceeding 2-3 g/d), the prevalence varied from 12.1% to 13.7%. When the cutoff value exceeded 1g/d, the prevalence of post-transplant proteinuria ranged from 7.5% to 40%. The highest prevalence of post-transplant proteinuria up to almost 50% was when the classic threshold for proteinuria (>150 mg/d) was used. Proteinuric patients have worse graft survival and mortality rates in comparison with non-proteinuric patients. Proteinuria also increases risk of cardiovascular events. Plenty of data suggest that proteinuria is associated with up to four times increased risk for graft failure. Roodnat et al. showed in their study that the risk for death increased by 16% (95% Confidence Interval [CI] 8 to 26%) for each 1.0 g/d increase in proteinuria.
Proteinuria is frequently seen immediately after transplantation. The reason can be the native kidney or the allograft, probably as a consequence of the ischemia-reperfusion injury. Proteinuria falls after successful kidney transplantation within few weeks. The residual or late proteinuria represents graft injury.
There are two main mechanisms which can cause proteinuria after kidney transplantation: an inadequate reabsorption of small proteins from proximal tubular cells and an increased passage of albumin or protein with higher molecular weight. The types and amounts of proteins appearing in the urine may indicate the specific transplant injury or pathologic condition. In post-transplant glomerular disease the proteinuria usually is nonselective with a high urinary immunoglobin G (IgG)/albumin rate. IgG is a highmolecular- weight protein (150 kd) that is not filtered in glomerulus under physiologic conditions because of pore width. By appearing in urine it reflects the intense glomerular injury and impairment of membrane selectivity. Proteinuria exceeding 1.5 g/d is a feature suggestive of glomerular disease as well. High levels of proteinuria are associated with transplant glomeroplathy, recurrent or de novo glomerulonephritis, focal glomerulosclerosis caused by chronic calcineurin inhibitors toxicity. Low-grade proteinuria up to 0.5 g/d would reflect tubular compartment injury. The diminished tubular reabsorption affects various low-molecular-weight proteins (21-kd retinol-binding protein, 12-kd β-2 microglobulin). The reasons of tubular proteinuria are acute rejection, ischemia-reperfusion injury, nephrotoxic agents (certain antibiotics, antiviral drugs). The Spare-the- Nephron trial showed that sirolimus significantly increases proteinuria in comparison with calcineurin inhibitors. The two types of proteinuria are interrelated. Glomerular damage may impact tubular interstitium and tubulointerstitial changes may create glomerular lesions. In advanced forms of transplant disease mixed (tubular and glomerular) patterns of proteinuria are frequently found. Hope you will Understand.
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Proteinuria is frequently seen immediately after transplantation. The reason can be the native kidney or the allograft, probably as a consequence of the ischemia-reperfusion injury. Proteinuria falls after successful kidney transplantation within few weeks. The residual or late proteinuria represents graft injury.
There are two main mechanisms which can cause proteinuria after kidney transplantation: an inadequate reabsorption of small proteins from proximal tubular cells and an increased passage of albumin or protein with higher molecular weight. The types and amounts of proteins appearing in the urine may indicate the specific transplant injury or pathologic condition. In post-transplant glomerular disease the proteinuria usually is nonselective with a high urinary immunoglobin G (IgG)/albumin rate. IgG is a highmolecular- weight protein (150 kd) that is not filtered in glomerulus under physiologic conditions because of pore width. By appearing in urine it reflects the intense glomerular injury and impairment of membrane selectivity. Proteinuria exceeding 1.5 g/d is a feature suggestive of glomerular disease as well. High levels of proteinuria are associated with transplant glomeroplathy, recurrent or de novo glomerulonephritis, focal glomerulosclerosis caused by chronic calcineurin inhibitors toxicity. Low-grade proteinuria up to 0.5 g/d would reflect tubular compartment injury. The diminished tubular reabsorption affects various low-molecular-weight proteins (21-kd retinol-binding protein, 12-kd β-2 microglobulin). The reasons of tubular proteinuria are acute rejection, ischemia-reperfusion injury, nephrotoxic agents (certain antibiotics, antiviral drugs). The Spare-the- Nephron trial showed that sirolimus significantly increases proteinuria in comparison with calcineurin inhibitors. The two types of proteinuria are interrelated. Glomerular damage may impact tubular interstitium and tubulointerstitial changes may create glomerular lesions. In advanced forms of transplant disease mixed (tubular and glomerular) patterns of proteinuria are frequently found. Hope you will Understand.
Thanks.
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