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Two forms of infection pose a special risk-bloodstream infection related to vascular access (including that for dialysis) and pneumonia doctor for erectile dysfunction in dubai purchase malegra fxt plus cheap, which puts the patient at high 526 Kidney Transplantation: Principles and Practice risk for subsequent lung infection with nosocomial organisms erectile dysfunction normal testosterone best malegra fxt plus 160 mg. Several other infections are commonly encountered and should be treated and cleared before transplantation erectile dysfunction diabetes qof malegra fxt plus 160 mg low price. Peritonitis must be cleared before surgery and infected peritoneal dialysis catheters removed erectile dysfunction 35 year old male buy malegra fxt plus online from canada. Urinary tract infection must be eliminated with antibiotics erectile dysfunction causes in young males order 160 mg malegra fxt plus mastercard, with or without nephrectomy. Similarly, skin disease threatens the integrity of a primary defense against infection and should be corrected even if doing so requires the initiation of immunosuppression. Finally, a history of more than one episode of diverticulitis should trigger an evaluation to determine whether colectomy is indicated before transplant. Strongyloides hyperinfection syndrome (hemorrhagic enterocolitis, pneumonia, gram-negative or polymicrobic bacteremia, or meningitis) may occur more than 30 years after transplantation. Patients from endemic areas should be screened and Strongyloides-seropositive recipients empirically treated (ivermectin) pretransplant to prevent active disease after transplant. The incidence of active and disseminated tuberculosis is higher in the transplant recipient than in the general population and the major antituberculous drugs are potentially hepatotoxic and some significantly interact with immunosuppressive agents. Patients at greater risk of tuberculosis infection or exposure include individuals with prior history of active tuberculosis or significant signs of old tuberculosis on chest radiograph, recent tuberculin reaction conversion, known exposure to active disease, protein-calorie malnutrition, cirrhosis, other immunodeficiency, or exposures related to living conditions. For those with latent infection, therapy should be initiated before transplantation although some judgment may be used as to the optimal timing of latent treatment. Given the potential toxicity of antimicrobial agents and the need for rapid interruption of infection, early, specific diagnosis is essential in this population. Whereas initial, empiric therapy is broad by necessity, a rapid narrowing of the antimicrobial spectrum as data become available is essential. In contrast, for intercurrent bacterial or fungal infections, reductions in immunosuppression might be reversed when resolution of infection is demonstrated. Even latent infection or low-level replication has important implications for transplant outcomes, and strategies used to prevent (universal versus preemptive therapy) and treat infection vary between centers. More accurate terms might be "viremic/cytopathic" effects and "cellular/immunologic" effects. Virus derived from a seropositive donor may reactivate in a seropositive recipient (D+/R+). Serologic tests are useful before transplantation to predict risk but are of little value after transplantation in defining clinical disease, because seroconversion is generally delayed. Chorioretinitis can occur at low levels of viral replication and generally later in the posttransplant course. Viremia and symptomatic infections are rare during effective antiviral prophylaxis. Over 50% of these patients become viremic in the absence of prophylaxis, often without symptoms. Many become viremic after cessation of antiviral prophylaxis, with symptomatic "late infection" occurring in up to one-third of recipients previously treated with prophylaxis. In reactivation infection, seropositive individuals reactivate endogenous virus after transplantation (D+ or D-/R+). When conventional 528 Kidney Transplantation: Principles and Practice developed: molecular and antigen detection assays. A single quantitative assay should be used consistently for monitoring each patient. Multiple viral genotypes may be observed, often in patients with more severe disease and in antiviral resistance. Resistance testing should be performed in the face of poor clinical and virologic response to adequate therapy for at least 10 to 14 days; responses may be delayed with high-level viremia. Multiple risk factors for drug resistance often coexist, including prolonged antiviral drug exposure; notably with inadequate dosing, lack of immunity, high-level viral replication; and intensive immunosuppression. In the high-risk patient (D+/R- or R+ with antilymphocyte globulin), after the completion of prophylaxis, monthly screening is performed to ensure the absence of viremia for 3 to 6 months. Preemptive therapy incurs extra costs for monitoring and coordination of outpatient care, while reducing the cost of drugs and the inherent toxicities. Many centers use a combination of both approaches: universal prophylaxis for the highest-risk recipients (D+/R- and R+ with T cell depletion) and preemptive therapy for others. Infrequently, breakthrough disease and ganciclovir resistance have been observed with both approaches. Other groups are candidates for preemptive therapy if an appropriate monitoring system is in place and patient compliance is good. Valganciclovir and ganciclovir are associated with neutropenia; however, dose reduction risks breakthrough viremia and the emergence of viral resistance. Given changing renal function after transplantation and the costs of medication, many regimens employ lower doses of valganciclovir. Relapse does occur, primarily in seronegative patients, in those with high viral burdens, if not treated to the achievement of a negative quantitative assay, and in gastrointestinal disease treated with an oral regimen. Repeat endoscopy may be considered with poor 31 · Infection in Kidney Transplant Recipients 529 clinical response, or if other processes are present (ischemia, cancer). In practice, it is reasonable to initiate therapy with intravenous ganciclovir, monitor weekly to assure a virologic response and treat until after monitoring is negative (often two negative weekly assays). Such patients may benefit from 2 to 4 months of oral valganciclovir (900 mg daily based on creatinine clearance) administered as secondary prophylaxis after the completion of intravenous therapy. This approach has resulted in rare symptomatic relapses and has been associated uncommonly with the emergence of antiviral resistance. It may be worth measuring a formal creatinine clearance to assure adequate dosing. Cidofovir may also be used, but often incurs significant nephrotoxicity and ocular toxicity. Letermovir appears to have good oral bioavailability, and a low rate of adverse effects and drug­drug interactions. Lymphomas constitute 15% of tumors among adult transplant recipients (51% in children) with mortality of 40% to 60%. Many deaths are associated with allograft failure after withdrawal of immunosuppression during treatment of malignancy. In kidney transplantation, the failure to regress with significant reductions in immunosuppression may suggest the need to sacrifice the allograft for patient survival. In such patients, the etiologies of decreased renal function must be carefully evaluated. Reduced immunosuppression may stabilize renal allograft function but risks graft rejection. Reactivation occurs with immunodeficiency and immunosuppression and tissue injury. The clinical presentation of disease is usually as asymptomatic, sterile pyuria, reflecting shedding of infected tubular and ureteric epithelial cells. These cells contain sheets of virus and are detected by urine cytology as "decoy cells. If screening is performed by plasma viral load, the interval between screening assays should be reduced to monthly for the first 6 months posttransplant. This reflects the faster onset of permanent renal injury in patients with circulating viremia compared with urinary excretion. It is useful to monitor the response to such maneuvers using plasma viral load measurements. General targets include tacrolimus trough levels of <6 ng/mL, cyclosporine trough levels <150 ng/mL, sirolimus trough levels of <6 ng/mL, and/or mycophenolate mofetil daily dose equivalents of 1000 mg. Regardless of the approach, renal function (at least 1­2 times per week), drug levels, and viral loads (alternate weeks) must be monitored carefully during reductions. Significant renal toxicity may be observed with cidofovir despite probenecid which may decrease efficacy. Some centers allow retransplantation after immunosuppression has been discontinued for some period. This infection may present with focal neurologic deficits or seizures and more slowly progressive neurologic lesions and may progress to death after extensive demyelination. Prophylaxis for opportunistic infections depends on the epidemiology of the individual. The drug of choice for documented Aspergillus infection is voriconazole, despite its significant interactions with calcineurin inhibitors and rapamycin. Although not as toxic as amphotericin B preparations, echinocandins can be used in situations where azole and polyene antifungals are contraindicated, but they are not recommended as primary therapy for invasive aspergillosis, including renal infections. Combination therapy using voriconazole and anidulafungin has been studied in the hematologic malignancy population but did not show a survival advantage. Surgical debridement is sometimes required for successful clearance of such invasive infections. These infections are usually treatable through correction of the underlying metabolic abnormality and topical therapy with clotrimazole or nystatin (see Table 31. Optimal management of Candida infection occurring in association with surgical drains or vascular access catheters requires removal of the foreign body and systemic antifungal therapy with fluconazole or echinocandin. A single positive blood culture result for Candida species necessitates systemic antifungal therapy; this finding carries a significant risk of dissemination in this population. A special problem in kidney transplant recipients is candiduria, including in asymptomatic patients. Notably in individuals with poor bladder function, obstructing fungal balls can develop at the ureteropelvic junction, resulting in obstructive uropathy, ascending pyelonephritis, and the possibility of systemic dissemination. Aspergillus Invasive aspergillosis is a medical emergency in the transplant recipient, with the portal of entry being the lungs and sinuses in more than 90% of patients and the skin in most of the others. Brain and epidural abscesses have been observed and may be particularly problematic when secondary to an antibiotic-resistant pathogen. As noted earlier, fungi may be metastatic from lungs but also may spread from sinuses, skin, and the blood. Cryptococcal infection is rarely seen in the transplant recipient until more than 6 months after transplantation. Cryptococcosis should be suspected in transplant recipients who present more than 6 months after transplantation with unexplained headaches (especially when accompanied by fevers), decreased state of consciousness, failure to thrive, or unexplained focal skin disease (which requires biopsy for culture and pathologic evaluation). Extended courses of fluconazole suppression may be required for patients based on clinical progress or net degree of immunosuppression. Such reactivation can result in either diarrheal illness or parasite migration with hyperinfection syndrome (characterized by hemorrhagic enterocolitis, hemorrhagic pneumonia, or both) or disseminated infection with accompanying (usually) gram-negative bacteremia or meningitis. Immigrants, refugees, travelers to and military personnel stationed in hyperendemic regions including Africa, Asia, Latin America, and the Caribbean should be screened with Strongyloides IgG serology before transplantation and should be treated with ivermectin preemptively if seropositive. Pneumocystis and Fever With Pneumonitis the spectrum of potential pulmonary pathogens in the transplant recipient is broad. The depressed inflammatory response of the immunocompromised transplant patient may greatly modify or delay the appearance of a pulmonary lesion on radiograph. Focal or multifocal consolidation of acute onset is likely to be caused by bacteria. Similar multifocal lesions with subacute to chronic progression are more likely secondary to fungi, tuberculosis, or Nocardia. Additional clues can be found by examining pulmonary lesions for cavitation, which suggests necrotizing infection as may be caused by fungi (Aspergillus or Mucoraceae), Nocardia, Staphylococcus, and certain gram-negative bacilli, most commonly Klebsiella pneumoniae and Pseudomonas aeruginosa. Atypical Pneumocystis infection (radiographically or clinically) may be seen in patients who have coexisting pulmonary infections or who develop disease while receiving prophylaxis with second-line agents. Alternative therapies are less desirable but have been used with success, including intravenous pentamidine, atovaquone, clindamycin with primaquine or pyrimethamine, and trimetrexate. The use of short courses of adjunctive steroids with a gradual taper is generally useful. Urinary Tract Infection Most urinary tract infections occur in the first year after kidney transplant. Urinary tract infection beyond 6 months after transplantation is associated with reduced renal graft survival and increased mortality. The risk for vesicoureteral reflux is dependent in part on the surgical approach to implantation of the ureter. The risk for candiduria is increased in patients who have received prior antimicrobial therapy, with neurogenic bladder, with indwelling urethral catheters, and in intensive care units. Most kidney transplant recipients with bacteriuria are asymptomatic, whereas pain with pyelonephritis represents transmural infection with local inflammation outside the denervated allograft causing what is perceived as allograft tenderness. The major causative organisms include gram-negative bacilli (Escherichia coli, Klebsiella, Pseudomonas, Enterobacter, Proteus) and gram-positives (largely enterococci) and fungi (Candida species). Each of these groups may manifest important antimicrobial resistance; therapy should be based on susceptibility patterns and by the presence or absence of structural abnormalities (obstruction, delayed bladder emptying). Initial empiric therapy should include antimicrobial agents not used previously for prophylaxis and, where possible, not used in prior episodes of infection given the risk for antimicrobial resistance. Short-course therapy is not used for treatment of uncomplicated urinary tract infection after transplantation; a 7-day minimum course with an effective agent is recommended. Upper tract disease (pyelonephritis) may require intravenous therapy initially and a 2- to 3-week total course. Asymptomatic candiduria should be treated in patients with renal allografts (although data are limited) with fluconazole (200 mg orally per day for 7­14 days). Upper tract disease with Candida species suggests obstruction and requires more intensive therapy (fluconazole 400 mg daily for 3­4 weeks). Echinocandins are not useful for treatment of most urinary tract infections because they achieve poor concentrations in the urine. Few recent studies address whether the changing ecology of bacteria has reduced the efficacy of prophylaxis.

The diagnosis should be suspected if the serum creatinine level is increasing (or not decreasing appropriately) erectile dysfunction pills for heart patients order 160 mg malegra fxt plus. Adjunctive tests to help make the diagnosis of urine leak fda approved erectile dysfunction drugs buy malegra fxt plus 160 mg low cost, if it is not obvious clinically impotent rage cheap 160 mg malegra fxt plus with mastercard, include a renal scan erectile dysfunction injections youtube malegra fxt plus 160 mg purchase overnight delivery, which would show urine in the retroperitoneal space surrounding the bladder or around loops of bowel erectile dysfunction drugs viagra discount malegra fxt plus master card, or an ultrasound, which would show a fluid collection outside the bladder and when aspirated has a high creatinine level. Urine leak generally is because of a surgical problem with the ureteroneocytostomy or ischemic necrosis of the distal ureter. Such a leak should be immediately repaired surgically because the risk of wound infection increases with delay in treatment. The aforementioned triad of clinical findings need not all be present, and the diagnosis should be suspected for any one of the three clinical signs. Magnetic resonance angiography usually can give an accurate delineation of the arterial anatomy. Ultrasound also is safe, but less discriminatory, and may be helpful if jetting of flow beyond a stricture is seen. As the population of renal transplant recipients has become older and includes more diabetic patients and patients with vascular disease, transplant renal artery pseudostenosis has become increasingly common. Pseudostenosis refers to arterial stenosis in the iliac artery proximal to the implantation of the transplant renal artery. Although the anastomosis and renal artery may be completely normal, a more proximal iliac artery stenosis can lead to hypoperfusion and resulting high renin output by the transplanted kidney. Treatment of transplant renal artery stenosis and pseudostenosis includes both percutaneous interventions and surgery. Generally, ostial stenosis, long areas of stenosis, and stenosis in tortuous arteries difficult to access radiographically are not treated as successfully with percutaneous interventions (balloon dilation or stenting) as with surgery. Stenoses within smaller branches of the renal artery may be treatable only by angioplasty. Iliac artery disease causing pseudostenosis may be treated by angioplasty, but risks embolization or dissection, leading to thrombosis or further ischemia. The patient was managed operatively by placing the kidney laterally in a retroperitoneal pocket and performing ureteroureterostomy using the ipsilateral native ureter. Occasionally, continuous bladder irrigation is necessary if gross hematuria is associated with clots, although intermittent manual irrigation usually is adequate. Bladder outlet obstruction by a blood clot is an emergency; vigilant nursing care is required to ensure that it does not occur. It is preferable not to distend the bladder in the immediate postoperative period to avoid disrupting the bladder sutures or causing a leak, and continuous bladder irrigation and cystoscopy ideally are avoided. Minor hematuria without clots is common in the first 1 or 2 days regardless of the surgical method of ureteroneocystostomy and does not require treatment; it resolves over time without specific treatment. Urine Leak A leak of urine from the transplanted kidney in the early postoperative period may be clinically obvious if the patient presents with abdominal pain, an increasing creatinine level, and a decrease in urine output. The risk of the procedure has to be weighed against the potential benefit of improving renal transplant blood flow. In addition to the serum creatinine determination, a biopsy may be useful to assess the quality of the renal parenchyma. In advanced chronic rejection with an elevated creatinine level for more than 1 month, it may not be prudent to repair such arteries, but this problem is not generally encountered in the early posttransplant course. Arterial Thrombosis Renal transplant arterial thrombosis usually occurs early (within 30 days) in the posttransplant period, but is a rare event and is generally caused by a technical error at the time of surgery. The diagnosis should be suspected in a patient who has had a transplant hours to days before and has had good urine output but who suddenly has a decrease in urine output. A high degree of suspicion has to be present, and the patient should be returned to the operating room promptly. Although some reports of catheterbased thrombolysis for renal artery thrombosis have been described, the majority of cases require operative intervention and if unsuccessful require transplant nephrectomy. The advantage of diagnostic ultrasound has to be weighed against the disadvantage of delaying a return to the operating room. Almost all kidney transplants with arterial thrombosis are lost because of ischemic injury. In cases of more than one renal transplant artery in which arterial reconstruction is performed at implantation, there may be increased risk of thrombosis of one or more arteries. This increased risk is a particular concern if there is a small accessory renal artery supplying the lower pole of the kidney and providing the ureteral blood supply. Thrombosis of a branch artery may manifest as an increase in serum creatinine levels associated with hypertension. Angiography shows partial thrombosis and loss of perfusion of a wedge-shaped section of renal parenchyma. The risk of this situation, in addition to potential long-term hypertension, is caliceal infarction and urine leak in the early postoperative period. Urine leaks occurring through the outer cortex of the kidney after partial infarction may be managed by nephrostomy tube placement for urinary drainage and placement of another drain adjacent to the kidney to prevent urinoma. When the transplant ureter necroses as a result of arterial ischemia, alternative urinary drainage needs to be provided surgically; this would be managed most often by ureteropyelostomy using the ipsilateral native ureter. Risk factors for renal vein thrombosis include use of the right donor kidney, prolonged ischemic time, older donors, older recipients, use of peritoneal dialysis pretransplant, hypercoagulable states in the recipient, and perioperative hypotension in the recipient. Immediate surgical repair of the vein and control of bleeding are required, and it is generally necessary to remove the kidney and revise the venous anastomosis. However, some instances of catheter-directed thrombolytic therapy or thrombectomy have been successfully reported 14 · Early Course of the Patient With a Kidney Transplant 203 long the kidney has been in place. If nephrectomy is performed within 4 weeks, there are minimal adhesions, and the vessels are exposed easily for ligation and transplant nephrectomy. At later times, it is usually easiest to reopen the transplant incision and enter the subcapsular plane around the kidney. The kidney is dissected free in the subcapsular space, and a large vascular clamp is placed across the hilum. The kidney is amputated above the clamp, and 3-0 polypropylene (Prolene) is used to oversew the hilar vessels. This kidney was enlarged to 14 cm in length with a surrounding fluid collection that represented blood. The condition was treated surgically with excision of the kidney, placement of a venous extension graft using donor iliac vein obtained from a third-party donor, and reimplantation of the kidney. Hyperacute rejection is now a rare event because of our understanding of transplant immunology and the implementation of more stringent immunologic testing of donors and recipients to prevent such occurrences. The incidence of hyperacute rejection is not 100% in those with preformed antibodies, presumably because some antibodies have lower affinity, lower density, do not bind complement, or cause accommodation. Bleeding generally occurs during the first 24 to 48 hours after transplantation and is diagnosed by a decreasing hematocrit, swelling over the graft with a bulging incision, or significant blood seepage from the incision. Postoperative bleeding occurs in roughly 12% of kidney transplant recipients and is more likely to occur in those with calcified iliac vessels who receive higher doses of heparin as prophylactic anticoagulation and in patients taking anticoagulation agents for other medical problems such as coronary artery or cerebrovascular disease. Otherwise, the systemic toxicity of a necrotic kidney may cause fever, graft swelling or tenderness, and generalized malaise. The technically easiest way to perform a transplant nephrectomy depends on how 204 Kidney Transplantation: Principles and Practice because type A2 expresses less of the putative antigen, but this strategy also has increased risk of graft loss. Desensitization regimens include the use of plasmapheresis combined with intravenous immunoglobulin and/or rituximab and are a growing area of research. A strategy such as this will maximize outcomes and utility for the kidney transplant community. The time course of this type of rejection is typically within days to weeks of the transplant, although it may occur at any time; it tends to be poorly responsive to steroids and occasionally resistant to all forms of antirejection therapy. Without adequate immunosuppression, acute rejection typically occurs 5 to 7 days after transplantation, but it can occur at virtually any later time. The clinical harbingers of acute rejection include an increasing creatinine level, weight gain, and graft tenderness. Often, there are no physical signs or symptoms, making the diagnosis largely dependent on laboratory assessment of renal function. Better diagnostics based on urine or blood molecular analysis have been developed but are at early stages of clinical application. First-line treatment of acute cellular rejection is bolus steroid therapy with methylprednisolone sodium succinate (Solu-Medrol). Many regimens are used successfully, but typical dose and duration are 10 mg/kg intravenously daily for 3 days (up to a maximum single dose of 500 mg/ day). However, antibody-depleting therapies may be associated with an increase in infectious complications when used to treat rejection compared with when used for induction. The effect of acute cellular rejection on graft survival depends on the response to treatment, with minimal effect if treatment results in return to baseline function but negative effect with incomplete response or repeated rejection episodes. It is thought to be a multifactorial process attributed to multiple donor and recipient factors that together mediate an ischemia-reperfusion injury that ultimately results in oxidative stress and an inflammatory cascade resulting in cell injury and death within the graft. The major differential diagnostic considerations in a recipient with decreasing or absent urine output are volume depletion or an acute vascular or urologic complication. This differential diagnosis can be evaluated with urgent ultrasound or radionuclide renal scanning. A biopsy of the kidney transplant should be performed to assess for rejection and acute tubular necrosis and is the gold standard for diagnosis. This situation may result in an alloimmune response, leading to an increased frequency of acute rejection. Generally, biopsies can be performed safely soon after transplantation, using real-time ultrasound imaging and automated biopsy needle devices. Monitoring cyclosporine and tacrolimus levels is valuable in preventing significant increases in blood levels, which may lead to nephrotoxicity. Antihypertensive medications should be used carefully in the posttransplant period to avoid hypotension, which may further worsen renal blood flow. Meticulous attention to daily weights, intake and output, and assessment of orthostatic blood pressure changes can diagnose volume depletion as a contributing factor to renal allograft dysfunction. Volume repletion with intravenous or oral fluids is indicated in the setting of prerenal azotemia from volume depletion in the postoperative kidney transplant recipient. Examples of the former include nonsteroidal antiinflammatory drugs and nephrotoxic antibiotics such as amphotericin and aminoglycosides. Selective serotonin reuptake inhibitor antidepressants are another class of pharmacologic agents that need to be used with care. Adjustment of the daily dose of cyclosporine and tacrolimus to attain therapeutic blood levels helps prevent episodes of nephrotoxicity from the concomitant use of these agents. Overuse of diuretics and uncontrolled blood glucose are two common causes of volume depletion and prerenal azotemia in the posttransplant kidney recipient. Electron microscopy of the allograft biopsy shows diffuse podocyte foot process effacement, which is diagnostic in this setting. Plasmapheresis alone or in combination with any of those treatments seems to be most effective with a 60% to 70% success rate for this strategy. Kidney biopsy specimens show fibrin deposition in the small arterioles of the kidney. The incidence of recurrence in this population ranges from 50% to 60% and generally occurs in the first month posttransplant. Other prophylactic agents include antifungal agents, such as fluconazole or clotrimazole troches, which can reduce the risk of mucosal Candida superinfection. Highly resistant organisms have been detected with increasing frequency in transplant patients. The investigational drugs oritavancin and telavancin are have been shown to have bactericidal activity against enterococci resistant to linezolid, daptomycin, and vancomycin. The increase in Candida infection seems to be caused by the routine use of clotrimazole or fluconazole to prevent Candida infection. Intravenous antibiotic use predisposes patients to fungal infection after transplantation. Infection with extended-spectrum beta-lactam-producing gram-negative bacteria is becoming more common, particularly in the urinary tract. When an infection occurs in the kidney transplant recipient, aggressive management is indicated. This management may include removal or replacement of central venous catheters or Foley catheters. Any intraabdominal fluid collections should be aspirated and drained if clinical suspicion for abscess is high. Urinary tract infections should be treated promptly, and the Foley catheter and ureteral stent should be removed as soon as possible. Cyclosporine, tacrolimus, and corticosteroids all may contribute to the development of hypertension. It may be difficult to ascertain the specific cause of hypertension after renal transplantation, because multiple factors may be working in tandem to cause elevated blood pressure in the recipient. The high incidence of hypertension in kidney transplant recipients and the fact that hypertension is an independent risk factor for cardiovascular disease in recipients warrants close monitoring and screening for hypertension in this high-risk population. Although there are no strong data or specific recommendations regarding the types of antihypertensives to use in this population, some observational studies have suggested avoiding calcium channel blockers in specific cases. Because of the complexity of this patient population, an individualized approach to blood pressure management and selection of the optimal antihypertensive for treatment is important. As discussed previously, persistently elevated or difficult to control blood pressures, along with signs of allograft dysfunction in the kidney transplant recipient, should prompt an additional workup for vascular compromise of the allograft with imaging. Early diagnosis and directed therapy are crucial in the early posttransplant period to initiate appropriate therapy and to avoid potential overimmunosuppression. Urine output, serum creatinine, and urine protein are all useful parameters to measure postoperatively to help identify graft dysfunction in the kidney transplant recipient.

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References

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