| DISEASE ASSOCIATIONS |
CHARACTERIZATION |
| AORTIC DISSECTION |
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The coexistence of acute aortic dissection with autosomal dominant polycystic kidney disease--description of two hypertensive patients.
Peczkowska M, Januszewicz A, Grzeszczak W, Moczulski D, Janaszek-Sitkowska H, Kabat M, Biederman A, Hendzel P, Prejbisz A, Cendrowska-Demkow I, Zielinski T, Januszewicz M.
Department of Hypertension, Institute of Cardiology, Warsaw, Poland.
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| Blood Press. 2004;13(5):283-6. Abstract quote |
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BACKGROUND: Acute aortic dissection is a rare but potentially lethal disease characterized by high early mortality when left untreated. However, survival may be significantly improved by the timely institution of appropriate medical and/or surgical therapy. Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common hereditary disorders, accounting for 8-10% of the cases of end-stage renal disease. Hypertension occurs frequently and is an early manifestation of ADPKD in approximately 50-70% of non-azotemic patients. ADPKD, often caused by mutations in the PKD1 gene, is associated with life-threatening vascular abnormalities that are commonly attributed to the frequent occurrence of hypertension.
METHODS: We present two cases of hypertensive patients with acute aortic dissection (type A Stanford) coexisting with ADPKD.
RESULTS: A 54-year-old male hypertensive patient and a 47-year-old male hypertensive patient, both with known ADPKD were diagnosed and operated with acute dissection of ascending aorta. Both patients were characterized by severe hypertension; therefore, in both cases, degree of hypertension is likely to be causative for this vascular complication. However, since ADPKD is associated with the vascular complications mentioned above, abnormality of the structure of the arterial wall of the thoracic aorta cannot be ruled out.
CONCLUSION: Aortic dissection is a rare but potentially disastrous complication, and clinicians should always consider this when dealing with patients with ADPKD who present with chest pain or collapse.
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| HYPERTENSION |
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Characteristics of hypertension in young adults with autosomal dominant polycystic kidney disease compared with the general U.S. population.
Kelleher CL, McFann KK, Johnson AM, Schrier RW.
Department of Medicine, University of Colorado School of Medicine, Denver, Colorado, USA.
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| Am J Hypertens. 2004 Nov;17(11 Pt 1):1029-34. Abstract quote |
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BACKGROUND: Patients with autosomal dominant polycystic kidney disease (ADPKD) often develop hypertension before any abnormalities in renal function are detected clinically. Therefore, standard screening (serum creatinine and urinalysis) of young individuals with unexplained hypertension to exclude renal parenchymal disease would rarely detect ADPKD.
METHODS: Data from 516 subjects with ADPKD (217 male and 299 female), aged newbornto 55 years with a normal serum creatinine and no proteinuria based on urine dipstick, studied between 1985 and 2000, were compared with data from similar subjects from the National Health and Nutrition Examination Survey (NHANES) III (1988-1994) and NHANES IV (1999-2000) data, by gender.
RESULTS: There was a highly significant occurrence of hypertension in young patients with ADPKD when compared to patients aged 20 to 34 years in the U.S. population. The hypertension in patients with ADPKD occurred in the absence of abnormal renal function or abnormal urinalysis.
CONCLUSIONS: These data indicate that renal ultrasound screening of young hypertensive individuals (aged 20 to 34 years) should be considered when searching for causes of secondary hypertension. Identifying affected ADPKD individuals early in their disease will permit aggressive blood pressure treatment and early inhibition of the renin-angiotensin-aldosterone system, which has been shown to reverse left ventricular hypertrophy, an important cardiovascular risk factor. In the present era of renal replacement therapy, cardiovascular complications are the main cause of death in patients with ADPKD.
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| POLYCYSTIC DISEASE OF THE LIVER |
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Polycystic disease of the liver.
Everson GT, Taylor MR, Doctor RB.
Division of Gastroenterology & Hepatology, University of Colorado School of Medicine, Denver, CO 80262, USA.
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| Hepatology. 2004 Oct;40(4):774-82. Abstract quote |
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Autosomal dominant polycystic disease is genetically heterogeneous with mutations in two distinct genes predisposing to the combination of renal and liver cysts (AD-PKD1 and AD-PKD2) and mutations in a third gene yielding isolated liver cysts (the polycystic liver disease gene). Transcription and translation of the PKD1 gene produces polycystin-1, an integral membrane protein that may serve as an extracellular receptor. Mutations occur throughout the PKD1 gene, but more severe disease is associated with N-terminal mutations. The PKD2 gene product, polycystin-2, is an integral membrane protein with molecular characteristics of a calcium-permeant cation channel.
Mutations occur throughout the PKD2 gene, and severity of disease may vary with site of mutation in PKD2 and the functional consequence on the resultant polycystin-2 protein. Polycystic liver disease is genetically linked to protein kinase C substrate 80K-H (PRKCSH). The PRKCSH gene encodes hepatocystin, a protein that moderates glycosylation and fibroblast growth factor receptor signaling. More prominent in women, hepatic cysts emerge after the onset of puberty and dramatically increase in number and size through the child-bearing years of early and middle adult life. Although liver failure or complications of advanced liver disease are rare, some patients develop massive hepatic cystic disease and become clinically symptomatic.
There is no effective medical therapy. Interventional and surgical options include cyst aspiration and sclerosis, open or laparoscopic cyst fenestration, hepatic resection, and liver transplantation.
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| PATHOGENESIS |
CHARACTERIZATION |
| GENERAL |
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Molecular Basis of Autosomal Dominant Polycystic Kidney Disease.
Al-Bhalal L, Akhtar M.
From the *Department of Pathology and Laboratory Medicine, King Khalid University Hospital, Riyadh, Saudi Arabia; and daggerDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, New York.
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| Adv Anat Pathol. 2005 May;12(3):126-133. Abstract quote |
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Autosomal dominant polycystic kidney disease (ADPKD) is a serious, life-threatening genetic disease in which extensive epithelial-lined cysts develop in the kidneys and, to a lesser extent, in other organs such as liver, pancreas, and ovaries.
In a majority of cases (80-85%), the gene involved is PKD1, which is located on chromosome 16 (16q13.3) and encodes polycystin-1, a large receptor-like integral membrane protein that contains several extracellular motifs indicative of cell-cell and cell-matrix interaction. In the remaining (10-15%) cases, the disease is milder and is caused by mutational changes in another gene (PKD2), which is located at chromosome 4 (4q21-23) and encodes polcystin-2, a transmembrane protein, which acts as a nonspecific calcium-permeable channel.
Both polycystins function together in a nonredundant fashion, through a common pathway, and produce cellular responses that regulate proliferation, migration, differentiation, and kidney morphogenesis. Through combined function of polycystins, normal tubular cells are maintained in a state of terminal differentiation, and their proliferation is strictly controlled
. Loss of function of either protein due to gene mutations results in the tubular cells reverting to a less differentiated state, which is more prone to proliferation. Patients with ADPKD carry a germ-line mutation in PKD1 or PKD2. A second somatic mutation in some of the tubular cells results in loss of both normal alleles, leading to loss of polycystin function. The affected cells lose the normal terminally differentiated state, revert to less differentiated phenotype, and undergo proliferation, which leads to cyst formation. As the cysts enlarge over many decades, the normal renal parenchyma is progressively destroyed, leading to renal failure.
Recently, the crucial role of primary cilia in modulating proliferation, migration, and differentiation of tubular epithelium has been recognized. Most of the tubular cells have one or two primary cilia projecting from the apical surface into the luminal space. The cilia act as mechanoreceptors as they bend with the urinary flow within the tubules. Both polycystins are strategically located within the cilia and act as important mediators of ciliary mechanosensation.
Loss of this important function due to mutational changes in PKD1 or PKD2 leads to loss of normal control over cellular proliferation, resulting in cyst formation. Several other ciliary proteins have recently been found to contribute directly to a wide spectrum of human kidney diseases with cystic phenotype, thus underscoring the pivotal role the primary cilia play in maintaining the normal structure and function of the tubular cells and probably other cells in the body.
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New insights into ADPKD molecular pathways using combination of SAGE and microarray technologies.
Husson H, Manavalan P, Akmaev VR, Russo RJ, Cook B, Richards B, Barberio D, Liu D, Cao X, Landes GM, Wang CJ, Roberts BL, Klinger KW, Grubman SA, Jefferson DM, Ibraghimov-Beskrovnaya O.
Functional Genomics, Genzyme Corporation, Framingham, MA 01701-9322, USA.
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| Genomics. 2004 Sep;84(3):497-510. Abstract quote |
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Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in the PKD1 or PKD2 gene, but cellular mechanisms of cystogenesis remain unclear.
In an attempt to display the array of cyst-specific molecules and to elucidate the disease pathway, we have performed comprehensive high-throughput expression analysis of normal and ADPKD epithelia in a two-step fashion. First, we generated expression profiles of normal and cystic epithelia derived from kidney and liver using serial analysis of gene expression (SAGE).
We found 472 and 499 differentially expressed genes with fivefold difference in liver and kidney libraries, respectively. These genes encode growth factors, transcription factors, proteases, apoptotic factors, molecules involved in cell-extracellular matrix interactions, and ion channels. As a second step, we constructed a custom cDNA microarray using a subset of the differentially regulated genes identified by SAGE and interrogated ADPKD patient samples. Subsequently, a set of differentially expressed genes was refined to 26 up-regulated and 48 down-regulated genes with ap value of <0.01.
This study may provide valuable insights into the pathophysiology of ADPKD and suggest potential therapeutic targets.
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Polycystic kidney disease--the ciliary connection.
Ong AC, Wheatley DN.
Sheffield Kidney Institute, Division of Clinical Sciences (North), University of Sheffield, S5 7AU, Sheffield, UK.
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| Lancet. 2003 Mar 1;361(9359):774-6. Abstract quote |
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CONTEXT: "Cystic degeneration" of the kidneys was first described pathologically in 1841 and "polycystic kidneys" as a clinical syndrome in 1888. The heritable nature in some families was noted in 1899, and autosomal dominant and recessive patterns of inheritance of polycystic kidney disease (PKD) were later recognised. Autosomal dominant PKD is one of the most common human genetic diseases and results from mutations in PKD1 or PKD2. These genes encode two proteins, polycystin-1 and polycystin-2.
STARTING POINT: Primary cilia are cellular organelles previously thought by some to be vestigial. New findings from several species, including algae, nematodes, and mice, implicate defects in structure or function of primary cilia as a possible common mechanism central to the development of some forms of recessive PKD. Two recent reports propose a causal link between ciliary dysfunction and autosomal dominant PKD. B Yoder and colleagues (J Am Soc Nephrol 2002; 13:2508-16) show that polycystin-1 and polycystin-2 are localised to primary cilia in cultured renal epithelial cells. S Nauli and colleagues (Nat Genet 2003; 33:129-37) show that polycystin-1 and polycystin-2 function as flow-sensitive mechanosensors in the same signal-transduction pathway.
WHERE NEXT? Cystic epithelial cells show many altered cellular properties, including changes in proliferation, apoptosis, adhesion, differentiation, polarity, extracellular matrix synthesis, and fluid transport. The next important steps in PKD research will be to define the physiological roles of primary renal cilia and how defects in ciliary structure and function lead to the development of a cystic phenotype in different forms of PKD.
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GROSS APPEARANCE/
CLINICAL VARIANTS |
CHARACTERIZATION |
| GENERAL |
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Autosomal recessive and dominant polycystic kidney diseases.
Sessa A, Righetti M, Battini G.
Nephrology and Dialysis Unit, District Hospital, Vimercate, Milan, Italy.
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| Minerva Urol Nefrol. 2004 Dec;56(4):329-38. Abstract quote |
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It is possible to identify renal cysts in several subjects by ultrasonography imaging techniques. Among the inherited polycystic kidney diseases we include autosomal recessive polycystic kidney disease (ARPKD) and autosomal dominant polycystic diseases such as von Hippel-Lindau disease, tuberous sclerosis complex (TSC1 and TSC2), and autosomal dominant polycystic kidney disease (ADPKD). ARPKD is a rare disease, related to PKHD1 gene, located on chromosome 6p21, that encodes a protein named polyductin/fibrocystin.
Pathoanatomical features are bilateral kidney involvement with multiple microcysts, and invariably liver involvement with portal and interlobular fibrosis. A single genetic defect leads to different degrees of renal and hepatic involvement with very different phenotypes and different clinical outcome, in the same family too. ARPKD clinically may show 4 different forms: perinatal, neonatal, infantile, and juvenile. ADPKD is much more frequent (1: 400-1000 live births), and can arise from mutations in 2 different genes, named PKD1 located on chromosome 16p13.3, and PKD2 located on chromosome 4q21-23. The proteins encoded by the PKD1 and PKD2 genes are named polycystins which play crucial roles in several biologic processes.
To explain the focal lesions that affected different organs and tissues the "double hit" theory has been proposed (germinal mutation plus somatic mutation on PKD1 or PKD2). Recently, biologic evidence documented the crucial role of the renal primary cilia on the formation of polycystins to induce cystogenesis. ADPKD may be clinically characterized by abdominal pain, hypertension, episodes of gross hematuria, headache, renal stones, aortic and cerebral aneurysms, mitral valve prolapse, and polycystic liver disease. ADPKD is slowly progressive disease responsible for up 10% of end stage renal failure (ESRF) in every country of the world. Male sex, PKD1 gene, episodes of gross hematuria, and the precocity and severity of hypertension play an important role in the progression of renal disease to ESRF.
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| VARIANTS |
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| HISTOLOGICAL TYPES |
CHARACTERIZATION |
| GENERAL |
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Polycystic kidney disease: a predominance of giant nephrons.
Grantham JJ.
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| Am J Physiol. 1983 Jan;244(1):F3-10. Abstract quote |
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Polycystic kidney disease is a bilateral disorder that affects approximately 200,000-400,000 persons in the United States. The most common form of the disease is inherited as an autosomal dominant trait (ADPKD). It typically causes renal insufficiency by the fifth or sixth decade of life.
The disease is characterized by the progressive enlargement of a portion of renal tubule segments (proximal, distal, loop of Henle, collecting duct). The tubules enlarge from a normal diameter of 40 microns to several centimeters in diameter, causing marked gross and microscopic anatomic distortion. The cause of the cystic change in the tubules is unknown, but current possibilities include obstruction of tubule fluid flow by hyperplastic tubule cells, increased compliance of the tubule basement membranes, and/or increased radial growth of cells in specific portions of the renal tubule.
Several studies show that the epithelia of the cysts continue to transport Na+, K+, Cl-, H+, and organic cations and anions in a qualitative fashion similar to that of the tubule segment from which they were derived. ADPKD, then, is a disease in which some gigantic renal tubules, over a period of several decades, impair the function of nonaffected nephrons and thereby lead to renal failure.
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| DIFFERENTIAL DIAGNOSIS |
KEY DIFFERENTIATING FEATURES |
| CYSTS |
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- Renal Cystic Diseases: A REVIEW.
Bisceglia M, Galliani CA, Senger C, Stallone C, Sessa A.
From the *Division of Anatomic Pathology and the daggerDivision of Nephrology and Dialysis, IRCCS "Casa Sollievo della Sofferenza" Hospital, San Giovanni Rotondo (FG), Italy; the double daggerDepartment of Pathology, Cook Children's Medical Center, Fort Worth, TX; the section signDepartment of Pathology and Laboratory Medicine, Children's & Women's Health Centre of British Columbia, Vancouver, Canada; and the parallelDivision of Nephrology and Dialysis, City Hospital, Vimercate-Milan, Italy.
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This review aims to assist in the categorization of inherited, developmental, and acquired cystic disease of the kidney as well as to provide a pertinent, up-to-date bibliography.
The conditions included are autosomal-dominant polycystic kidney disease, autosomal-recessive polycystic kidney disease, unilateral renal cystic disease (localized cystic disease), renal simple cysts, multicystic dysplastic kidney, pluricystic kidney of the multiple malformation syndromes, juvenile nephronophthisis and medullary cystic disease, medullary sponge kidney, primary glomerulocystic kidney disease, and glomerulocystic kidney associated with several systemic disorders mainly of genetic or chromosomal etiology, cystic kidney in tuberous sclerosis, and in von Hippel-Lindau syndrome, cystic nephroma, cystic variant of congenital mesoblastic nephroma, mixed epithelial stromal tumor of the kidney, renal lymphangioma, pyelocalyceal cyst, peripylic cyst and perinephric pseudocyst, acquired renal cystic disease of long-term dialysis, and cystic renal cell carcinoma and sarcoma.
Whereas the gross and histologic appearance of some of these conditions may be diagnostic, clinical and sometimes molecular studies may be necessary to define other types.
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| CYSTIC HAMARTOMA |
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Cystic hamartoma of the renal pelvis.
Yoshida S, Nakagomi K, Goto S, Ozawa T.
Department of Urology, Hamamatsu Medical Center, Hamamatsu, Shizuoka 432-8580, Japan.
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| Int J Urol. 2004 Aug;11(8):653-5. Abstract quote |
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Cystic hamartoma of the renal pelvis is a rare benign tumor in the same category as mixed epithelial and stromal tumors.
We present a 33-year-old woman with a solid and cystic intrarenal tumor extending into the renal pelvis. She underwent radical nephrectomy and ureterectomy under the diagnosis of renal tumor or renal pelvic tumor.
Histopathologically, the tumor was composed of a biphasic proliferation of epithelial and mesenchymal elements. We believe the present case is best classified as a cystic hamartoma of the renal pelvis in the category of mixed epithelial and stromal tumors because of the coexistence of hamartomatous lesions, such as the proliferation of adipose cells and well to poorly differentiated fibromuscular lesions.
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| MEDULLARY CYSTIC DISEASE |
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Clinico-pathologic findings in medullary cystic kidney disease type 2.
Bleyer AJ, Hart TC, Willingham MC, Iskandar SS, Gorry MC, Trachtman H.
Section on Nephrology, Wake Forest University School of Medicine, Medical Center Blvd., Winston-Salem, NC, USA,
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| Pediatr Nephrol. 2005 Jun;20(6):824-7. Epub 2005 Apr 21. Abstract quote |
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Medullary cystic kidney disease type 2 is an uncommon autosomal dominant condition characterized by juvenile onset hyperuricemia, precocious gout and chronic renal failure progressing to end-stage renal disease in the 4th through 7th decades of life. A family suffering from this condition is described. The patient in the index case presented with renal insufficiency as a child.
A renal biopsy revealed tubular atrophy, and immunohistochemical staining of the tissue for uromodulin (Tamm Horsfall protein) revealed dense deposits in renal tubular cells. Genetic testing revealed a single nucleotide mutation (c.899G>A) resulting in an exchange of a cysteine residue for tyrosine (C300Y).
Medullary cystic kidney disease type 2 (also known as uromodulin-associated kidney disease) likely represents a form of endoplasmic reticulum storage disease, with deposition of the abnormal uromodulin protein in the endoplasmic reticulum, leading to tubular cell atrophy and death.
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| PROGNOSIS |
CHARACTERIZATION |
| MALIGNANCIES |
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Erythropoietin-producing renal cell carcinoma arising from autosomal dominant polycystic kidney disease.
Hama Y, Kaji T, Ito K, Hayakawa M, Tobe M, Kosuda S.
Department of Radiology, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, Japan.
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| Br J Radiol. 2005 Mar;78(927):269-71. Abstract quote |
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Erythropoietin (EPO)-producing renal cell carcinomas (RCC) in patients with chronic renal failure secondary to autosomal dominant polycystic kidney disease (ADPKD) has not previously been reported.
We report a case of EPO-producing RCC associated with ADPKD in a 66-year-old woman, and discuss the clinical and radiological findings.
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Renal sarcoma associated with adult polycystic kidney disease. A case report and literature review.
Minardi D, Mantovani P, Dellabella M, Dell'Atti L, Mazzucchelli R, Santinelli A, Scarpelli M, Muzzonigro G.
Institute of Urology, Polytechnic University of the Marche Region, Ancona, Italy.
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| Arch Ital Urol Androl. 2004 Jun;76(2):94-6. Abstract quote |
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The development of renal cell carcinoma in Adult Polycystic Kidney Disease (APKD) has been reported in the literature; one of the features of renal malignancy in APKD is the difficulty to make a diagnosis, and the majority of cases reported are incidental findings at surgery or autopsy.
We report a rare case of renal sarcoma in a patient with APKD. Sarcoma associated with APKD does not seem to have particular biological characteristics when compared with primary renal sarcoma; however the polycystic kidney represents an aggravating circumstance, because of the difficulty in making an early diagnosis of a disease with a poor prognosis.
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| TREATMENT |
CHARACTERIZATION |
| GENERAL |
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| NEPRHECTOMY |
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Unilateral nephrectomy as palliative therapy in an infant with autosomal recessive polycystic kidney disease.
Shukla AR, Kiddoo DA, Canning DA.
Division of Pediatric Urology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399, USA.
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| J Urol. 2004 Nov;172(5 Pt 1):2000-1. Abstract quote |
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Prenatal diagnosis of autosomal recessive polycystic kidney disease (ARPKD) implies a dire prognosis. Neonates affected by the more severe variants of ARPKD suffer respiratory failure caused by massive kidneys that restrict diaphragmatic expansion and result in pulmonary hypoplasia.
Afflicted infants who survive the neonatal period and gain adequate respiratory function may subsequently suffer from an inability to tolerate enteral nutrition due to abdominal compression from the massive kidney and the systemic effects of renal compromise. Palliative unilateral or bilateral nephrectomy may be considered in rare instances to facilitate pulmonary expansion and gastrointestinal function.
We report on an infant with severe ARPKD who was able to tolerate enteral nutrition only after left nephrectomy.
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| TRANSPLANTATION |
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Pretransplant nephrectomy in patients with autosomal dominant polycystic kidney disease.
Rozanski J, Kozlowska I, Myslak M, Domanski L, Sienko J, Ciechanowski K, Ostrowski M.
Pomeranian Medical University, Szczecin, Poland.
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BACKGROUND: Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disease and a frequent cause of end-stage renal failure. Transplantation in patients with ADPKD is associated with specific cyst-related problems, especially urinary tract infections (UTI). Although pretransplant nephrectomy has been applied in this group of patients, evidence of the benefits of this strategy is lacking. Therefore, we compared the outcomes and posttransplant complications among patients with or without pretransplant nephrectomy.
PATIENTS AND METHODS: ADPKD patients (73) transplanted from cadaveric donors were reviewed retrospectively with regard to posttransplant complications and outcomes. The groups either underwent pretransplant unilateral nephrectomy (n = 30) or were transplanted with native kidneys intact (n = 43).
RESULTS: Two patients underwent simultaneous bilateral nephrectomy due to a large size of the polycystic kidneys interfering with the transplant operation. Overall postransplant complications were more frequent in the group without nephrectomy (34% vs 20%); however, the difference was not statistically significant. Most complications were related to cyst infections with 3 deaths (12%) due to lethal septicemia in the group without nephrectomy. No infection-related deaths were noted in the group with pretransplant nephrectomy.
CONCLUSIONS: Graft and patient outcomes as well postransplant complications were similar in both groups, independent of previous nephrectomy. It seems that pretransplant unilateral nephrectomy should not be routine and has no advantage over transplantation with both native kidneys intact, although this conclusion is limited by the small number of patients. An Individualized approach should be applied especially when there has been a history of cyst-related infection.
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Transplantation of a cadaveric polycystic kidney in a patient with autosomal dominant polycystic kidney disease: long-term outcome.
Powell CR, Tata S, Govani MV, Chien GW, Orvieto MA, Shalhav AL.
Department of Urology, University of Illinois at Chicago, Chicago, Illinois, USA.
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| Transplant Proc. 2004 Jun;36(5):1288-92. Abstract quote |
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INTRODUCTION: Kidneys from donors affected by autosomal dominant polycystic kidney disease (ADPKD) were considered unusable for transplantation. To the best of our knowledge, seven cases worldwide have now been described in the English literature since 1967 suggesting such donor organs may be acceptable under certain conditions. Most of these reports have only short-term follow-up.
METHODS: We provide a review of these patients and share our experience with an ADPKD patient who had a cadaveric ADPKD transplant and has been closely followed for 10 years.
RESULTS: During the 10-year period, the patient had three transplant biopsies without complication. This creatinine is currently 1.2 mg/dL. Serial computed tomography imaging indicated that the cystic disease slowly progressed during this time period. He eventually developed intractable pain in his native left kidney and underwent a laparoscopic nephrectomy.
CONCLUSIONS: Normal functioning cadaveric kidneys that show early signs of polycystic kidney disease should be considered acceptable for renal donation. These organs provide the recipient a safe, reasonable period of graft survival and have not been shown to cause adverse effects.
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