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Ready for your vacation in paradise? Recent improvements in short-term graft survival rates have resulted in a larger number of patients being exposed to the risks of late complications 5 , Maximization of long-term patient survival rates requires the ongoing management of cardiovascular disease CVD risk factors, such as hyperlipidemia and hypertension, as well as screening for cancer and other complications that are directly or indirectly linked to immunosuppression. Because of the complexity of current immunosuppressive regimens and the high incidence of adverse drug effects and drug interactions, an experienced transplant physician should be involved in the long-term care of transplant recipients.

There are a number of reasons why relatively frequent visits to the transplant center may improve long-term outcomes. Chronic allograft failure, death with a functioning allograft, and nonadherence account for the great majority of late graft losses. The effects of each of these factors may be diminished by frequent visits to the transplant center.

With respect to nonadherence, effective immunosuppressive regimens have greatly reduced early graft loss and have enabled a growing number of recipients to achieve long-term graft survival, despite the fact that they remain at high risk for allograft rejection. It is ironic that the effectiveness of immunosuppressive medications administered to prevent early rejections has resulted in more recipients being dependent on these potent drugs to maintain long-term graft function.

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Consequently, the relative effects of nonadherence on graft outcomes is becoming greater 19 , 20 , Data gathered in other fields of medicine confirm the importance of frequent encounters between patients and providers in facilitating adherence to therapy. Therefore, efforts to decrease the frequency of outpatient visits to the transplant center or other providers may be counterproductive. Some data indicate that patients actually dislike long periods between visits; such gaps tend to foster uncertainty regarding the status of the allograft and worries about potential adverse outcomes.

Most but not all of the adverse consequences of renal failure can be directly attributed to insufficient GFR.

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Although other functions of the kidney are important, failure of these other functions is rarely observed in the absence of reduced GFR. Epidemiologic studies using large transplant registries have unequivocally demonstrated a progressive loss of renal allografts in the late posttransplant period. Therefore, only patients who die with a functioning allograft will likely escape a decrease in GFR at some time after transplantation.

The function of the transplant needs to be estimated repeatedly during the life of the graft. Episodes of acute allograft rejection have been documented in the third decade after transplantation, and allografts are constantly threatened by nonimmunologic injures that may or may not be reversible. At no time after transplantation can function stability be taken for granted. Clinical signs of rejection and dysfunction are notoriously unreliable, and repeated laboratory testing is required. There are a number of circumstances in which screening for graft dysfunction may alter therapy and benefit the patient.

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The first is the detection of acute rejection. Generally, the only practical way to detect acute rejection in its early treatable stage is to screen at regular intervals with some direct or indirect measurement of renal function. Acute rejection often occurs without signs or symptoms. Frequent repetitive allograft biopsies or fine-needle aspiration biopsies are theoretically possible but are less practical.

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  4. The early recognition of acute rejection and its complete reversal may minimize its unfavorable effects on long-term graft function. The completeness of reversal of graft dysfunction after an episode of acute rejection, as measured by the serum creatinine level, is a prognostic indicator. The second case is the detection of nephrotoxicity resulting from immunosuppressive medications. Cyclosporine A CsA and tacrolimus have become mainstays of immunosuppression after renal transplantation.

    Both can cause renal toxicity. As in the case of acute rejection, nephrotoxicity can be detected only by screening for changes in renal function. The detection of nephrotoxicity may prompt changes in immunosuppressive medications. Even small changes in the doses of immunosuppressive medications may cause changes in graft function. The third case is the detection of changes in renal function resulting from obstruction, renal artery stenosis, or other reversible causes of graft dysfunction.

    Other causes of graft dysfunction may be reversible if detected early and may be detected only if screening tests of renal function are routinely performed. In the fourth case, chronic renal allograft failure is often evident only from subtle changes in renal function. With time, all kidney transplants are subject to chronic allograft failure, which may occur as early as 6 mo after transplantation Although there is no proof from randomized controlled trials, an increasing amount of evidence suggests that aggressive risk-factor management may help slow the rate of progression of chronic allograft failure 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , Controlling BP, reducing urinary protein excretion, treating hyperlipidemia, and maximizing immunosuppression may help slow the rate of progression.

    Repetitive measurements of renal function may indicate patients with early chronic allograft failure and thereby identify patients who require close management and supervision. In addition, measurements of the rate of progression may help patients and caregivers plan for the eventual need for renal allograft replacement therapy.

    Finally, it is likely that measuring renal function is a helpful reminder to patients of the possibility of allograft dysfunction and regular measurements of renal function may help encourage patients and remind them to adhere to therapy. At least one study noted that the failure of patients to adhere to prescribed serum creatinine screening was a predictor of late renal allograft failure Measurement of serum creatinine levels is a simple and inexpensive but invaluable indirect method to detect decreases, especially acute decreases, in GFR.

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    The universal availability of laboratories that can measure serum creatinine levels makes this test particularly useful. The serum creatinine level is also the most valuable prognostic marker of subsequent graft function at all times after transplantation. The interval for measuring serum creatinine levels can be based on the frequency of expected graft dysfunction at different times after transplantation.

    Most cases of acute rejection and episodes of graft dysfunction occur in the first 2 mo after transplantation. Pediatric renal transplant recipients experience more acute rejection episodes than do adults 12 , This may be attributable to increased metabolism of immunosuppressive medications, heightened immune responses, or medication nonadherence. The incidence of late acute rejections may also be higher.

    As a result, children require more frequent surveillance. The normal range for serum creatinine levels changes with age and body size. Notwithstanding the practical advantages of using the serum creatinine level as a marker of renal function, it is a relatively inaccurate indicator of the true GFR for renal transplant recipients 33 , 34 , With formulas that take into account clinical parameters that are correlated with muscle mass, serum creatinine levels may more accurately reflect GFR 36 , 37 , 38 , 39 , However, GFR estimated by using formulas that include serum creatinine levels are also subject to substantial variability 41 , 42 , In addition, many of the variables used in formulas to estimate GFR e.

    The latter differences are most critical in the monitoring of renal transplant recipients. However, during long periods of time, changes in muscle mass and the resulting changes in creatinine production make the serum creatinine level a less sensitive marker for detecting chronic decreases in GFR Indeed, studies have demonstrated that the serum creatinine level is relatively unreliable for detecting chronic changes in renal function 33 , 34 , Other endogenous markers of GFR, such as the serum cystatin C level 46 , may ultimately prove to be superior to the serum creatinine level for detecting acute and chronic changes in renal function, but these markers require additional testing before they are adopted in routine clinical practice Urinary creatinine clearance determinations may be even less accurate than serum creatinine measurements.

    This is largely attributable to the difficulty of obtaining accurate timed urine collections. In addition, tubular secretion of creatinine results in systematic overestimation of the true GFR for renal transplant recipients 42 , This overestimation of the GFR can be reduced by blocking tubular secretion of creatinine with cimetidine 49 , 50 , 51 , Nevertheless, the usefulness of urinary creatinine clearance measurements is limited.

    Urinary and plasma clearance methods that use isotopic or nonisotopic markers of GFR are most accurate. Plasma clearance tests are relatively simple to perform and do not require accurate and difficult-to-obtain urine collections. Even methods that use only a single plasma sampling time after injection are reasonably accurate and generally acceptable for clinical practice 48 , 53 , Although clearance of isotopic agents can also be measured with a gamma camera positioned over the allograft 55 , 56 , this approach is more cumbersome and expensive.

    It can be argued that the detection of chronic decreases in GFR is not critical for the treatment of transplant recipients, because few therapeutic options are available. This line of reasoning holds that it is generally not necessary to routinely measure renal function by more accurate techniques that use isotopic or nonisotopic markers of GFR.

    However, these tests may be valuable to assess the significance of changes in serum creatinine levels with time and to provide more accurate baseline levels for follow-up monitoring. A growing body of evidence albeit largely circumstantial suggests that at least some therapies may delay the progression of chronic allograft failure 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , Therefore, detecting even small, gradual, progressive decreases in GFR may prompt patients and caregivers to be even more diligent in managing immunologic and nonimmunologic risks for graft failure.

    Finally, these more accurate techniques are often needed to assess the true GFR in planning for subsequent dialysis or repeat transplantation. Transient proteinuria is common and is often observed in association with episodes of acute allograft rejection. Transient proteinuria may not affect allograft or patient survival independent of its underlying cause. A number of epidemiologic studies have examined the incidence of persistent proteinuria among renal transplant recipients.

    The capacity to excrete urine that is virtually free of filtered protein is a critical function of healthy kidneys. Proteinuria is a manifestation of renal dysfunction and, when heavy, has important consequences for extracellular fluid volume regulation. The degree of proteinuria also has prognostic and diagnostic implications.

    Heavy proteinuria is often associated with more rapid deterioration of renal function and is more likely to be associated with pathologic glomerular lesions than with interstitial lesions or anatomic or hemodynamic causes of renal dysfunction 10 , 59 , 60 , 62 , 63 , 64 , 65 , The most common causes are chronic allograft nephropathy and recurrent or de novo glomerulonephritis 57 , 58 , 59 , 60 , 61 , 62 , 63 , Recurrent diabetic nephropathy is likely to become an increasingly common cause of proteinuria as the number of diabetic patients with long-term graft survival increases.


    Recently, experimental data suggested that proteinuria itself may cause renal injury 68 , Therefore, it is possible that the often-reported clinical association between proteinuria and the rate of renal function decrease 70 could be, in part, a direct result of injurious effects of proteinuria.

    A number of studies in the general population have suggested that proteinuria is an important risk factor for CVD 71 , 72 , Indications for and methods of screening for proteinuria were recently reviewed in a position paper by the National Kidney Foundation The prevalence of proteinuria among renal transplant recipients is high enough to give screening tests sufficient positive and negative predictive values. The consequences of new-onset persistent proteinuria are of sufficient magnitude to make screening a useful prognostic test.