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PubMed1976

Successful allotransplantation of a kidney removed because of ureteral damage in an unrelated living donor.

The use of a kidney removed because of ureteral damage in an unrelated donor has produced a well functioning renal allograft in the transplant recipient. The kidney demonstrated calicectasis and hydronephrosis on an excretory urogram before removal of the ureteral cutaneous fistula. An excretory urogram performed 8 months after the renal allotransplantation of this kidney shows prompt function of a delicate collecting system without any residual calicectasis. This case emphasizes the need for us to explore the possible use of free kidneys removed from living unrelated donors for non-neoplastic diseases of the ureter.

Adult↗

PubMed1985

Why do patients with lupus nephritis die?

Over 20 years 42 of 138 patients with systemic lupus erythematosus "died"--that is, suffered actual death or went into terminal renal failure, or both; data from 41 were available for analysis. In most patients the causes of death were multiple. Twenty seven patients went into terminal renal failure, of whom 25 were offered dialysis treatment. Three regained renal function later, 12 survived on dialysis or with functioning kidney allografts--almost all with inactive lupus--but 13 died after starting dialysis, most within a few weeks or months. The principal causes were active lupus or infection. In those patients with renal failure after rapid deterioration in renal function (n = 14) there were nine deaths, while of 10 patients with a slow evolution into renal failure, only four died. Four patients with impaired and 10 with normal renal function died, again most often from complications of lupus or from infection. Vascular disease was a major cause of death in seven patients, all but two of whom were young; of 15 postmortem examinations, eight showed severe coronary artery atheroma, and three surviving patients required coronary bypass operations. Analysis of the timing of death or entry into renal failure showed that in 12 out of 13 patients who died within two years of onset the lupus was judged to be active, while this was true in only eight out of 19 patients who died later. Six of the seven vascular deaths occurred later than two years from onset, while only nine of 26 renal "deaths" occurred before two years; deaths from infections (n = 13) were distributed equally. Despite this and aggressive treatment of active disease, the principal cause of actual death was uncontrolled lupus.

Adolescent↗

PubMed2003

Immune protection of auxiliary liver to other allograft: report of 3 cases.

OBJECTIVE: To assess the immune status of auxiliary liver transplantation and to clarify the immune protection of auxiliary liver to other allograft. METHODS: Immunological markers and pathological changes in 3 patients undergoing auxiliary liver transplantation were analysed. RESULTS: The lower the concentration of immunosuppressive agent, the less the rejection and the milder the intensity in the 3 patients. The function of allograft after auxiliary liver transplantation was excellent. CONCLUSIONS: Patients are in a low immune reaction state after auxiliary liver transplantation. Auxiliary liver can protect other allografts by related immunological mechanisms. The side-effects of low-concentration immunosuppressive agents on auxiliary liver and other allografts are mild.

Adult↗

PubMed2001

Adenine phosphoribosyltransferase deficiency and renal allograft dysfunction.

Adenine phosphoribosyltransferase (APRT) deficiency is a rarely diagnosed cause of renal allograft dysfunction. We report the case of a 42-year-old man who presented in 1996 with idiopathic renal failure. Native kidney biopsy showed extensive microcrystalline interstitial nephritis. The patient subsequently underwent a living-related kidney transplant with excellent early graft function. During the next year, however, he had worsening allograft function, and allograft biopsy showed recurrent interstitial nephritis. Further chemical and spectroscopic analysis showed this lesion to be an annular microcrystalline nephritis consistent with APRT deficiency. This diagnosis was confirmed on erythrocyte assay. Treatment with allopurinol and a low-purine diet led to improvement and stabilization of renal function. APRT is a rare cause of renal allograft dysfunction requiring a high index of suspicion for early diagnosis and treatment. Increased physician awareness in the United States may hasten diagnosis and limit the morbidity associated with this disease.

Adenine Phosphoribosyltransferase↗

PubMed2005

The significance of Tc-99m DTPA renal scintigraphy for the demonstration of progressive functional changes that accompany chronic allograft nephropathy.

OBJECTIVES: Chronic allograft nephropathy (CAN) is usually progressive; its natural course can only be modified in the initial stages. In this study, we graded Tc-99m diethylenetriaminepentaacetic acid (DTPA) renogram curves with respect to the perfusion/uptake pattern and correlated these findings with biopsy results in patients with CAN. METHODS: This study included 63 renal allograft recipients with biopsy-proven CAN. The agent used for renal scintigraphy was Tc-99m DTPA. Quantitative evaluation of perfusion included calculation of the ratio of peak perfusion counts divided by plateau counts (P:PL). Deterioration of renal function was accompanied with a gradual loss of a peak and plateau pattern. For the evaluation of uptake in relation to perfusion pattern, we graded the renogram curves into four based on the presence of a peak and plateau pattern and the presence of an uptake peak. RESULTS: In patients with CAN, the mean P:PL was significantly lower than that of the control group. The serial changes in successive grades of CAN in respect to uptake-perfusion pattern was a gradual loss of peak and plateau pattern followed by a decline in uptake. In recipients with high-grade CAN, an uptake peak was absent. CONCLUSIONS: Evaluation of Tc-99m DTPA time-activity curves revealed a progressive change in perfusion-uptake pattern in patients with CAN. According to our results, deterioration of perfusion preceded the decline in uptake. Serial renogram changes are thought to reflect initial hypoperfusion followed by increased intraglomerular pressure and finally glomerulosclerosis. These findings have implications for the pathophysiology and management of CAN.

Biopsy↗

PubMed2004

Association of Fc gamma receptor IIA polymorphisms with acute renal-allograft rejection.

Acute rejection is a leading cause of early renal-allograft failure. The human Fc gamma receptor IIA (FcgammaRIIA) forms an essential link between the humoral branch and the effector cells of the immune system. In this study, we examined FcgammaRIIA genotypes in renal-allograft recipients (rejectors) with acute graft rejection and in a number of control groups to investigate a possible association between FcgammaRIIA polymorphism and acute renal-allograft rejection. The distribution of the genotypes in the study patient group differed from the control groups. The frequency of homozygosity for FcagammaRIIA-R/R131 in the rejectors was significantly higher than that in the recipients (nonrejectors) with well-functioning renal allografts and in blood donors (P< 0.05). In comparison with the control groups, the rejectors displayed a higher R131 allele frequency (P< 0.05) and a lower H131 allele frequency (P< 0.05). These results reveal a significant association between FcgammaRIIA-R/R131 and acute renal-graft rejection, and it is likely that FcgammaRIIA polymorphisms could be useful markers for potential risk of rejection.

Adult↗

PubMed2001

Early glomerular dysfunction in human renal allografts.

BACKGROUND: The long-term outcome of renal allografts is characterized by a progressive deterioration of renal function and graft loss. Our aim was to determine early glomerular functional abnormalities, before they become clinically apparent. METHODS: Glomerular hemodynamics and dextran sieving were characterized in 21 well-functioning cadaveric renal allograft recipients [normal glomerular filtration rate (GFR) and albumin excretion rate (AER), who also had a kidney biopsy with normal or minimal histological changes] and in 15 uninephrectomized kidney donors. Both groups were one to three years after transplantation or uninephrectomy. RESULTS: The GFR and renal plasma flow (RPF) were similar in both groups (62 +/- 3 vs. 63 +/- 4, and 343 +/- 26 vs. 334 +/- 21 mL/min/1.73 m2 for GFR and RPF, in cadaveric recipients vs. donors, respectively), the AER was normal in both groups, but the mean arterial pressure was higher in renal recipients (103 +/- 3 vs. 94 +/- 3 mm Hg in uninephrectomy controls, P < 0.05). Despite similar levels of overall glomerular function in the two groups, the dextran sieving curve was uniformly elevated in the renal allograft recipients versus uninephrectomy controls (P < 0.05 for dextrans 38 to 66 A). Using a log-normal glomerular pore-size distribution model to analyze potential mechanisms, the elevation in the dextran sieving curve resulted from a shift in the distribution of glomerular filtering pores to a larger size (mean glomerular pore size 46 +/- 2 vs. 43 +/- 2 A for uninephrectomy controls, P < 0.05), resulting in a larger fraction of filtrate volume permeating very large pores. By morphometric analysis, the thickness of the glomerular basement membrane was increased in kidney allograft as compared to 2-kidney biopsy controls (614 +/- 33 vs. 427 +/- 22 nm, respectively, P < 0.05). CONCLUSIONS: Even in "well functioning" renal allografts there is a glomerular dysfunction characterized by increased permeability to macromolecules resulting from a shift of the glomerular pores to a larger size. These changes could be mediated by ultrastructural alterations at the glomerular capillary or by alterations in intraglomerular hemodynamics. Early allograft dysfunction may contribute to the progressive renal insufficiency of renal allografts.

Adolescent↗

PubMed1993

Induction of donor-specific unresponsiveness to rat cardiac allografts by pretreatment with intrathymic donor MHC class I antigens.

Since intrathymic injection of UV-B-irradiated spleen cells induces donor-specific unresponsiveness in the sublethally irradiated (200 rads TBI) recipients, while intrathymic injection of naive SC leads to acute graft rejection, we hypothesized that presentation of MHC class I rather than MHC class II antigens to immature T cells in the thymus may convey a tolerogenic signal to the recipient. The present study was designed to examine if intrathymic injection of naive MHC class I-positive resting T lymphocytes can induce antigen-specific unresponsiveness to cardiac allografts in the Lewis-to-ACI rat combination. The results showed that intrathymic injection of resting Lewis T cells consistently induced indefinite graft survival (> 300 days) in sublethally irradiated (200 rads TBI) ACI recipients while similar treatment failed to prevent the rejection of third-party (Wistar-Furth) cardiac allografts, thus demonstrating the specificity of the immunologic unresponsiveness to donor alloantigens. Examination of the timing of intrathymic antigen presentation relative to cardiac transplantation that would achieve 100% permanent graft survival in the Lewis-to-ACI rat combination showed that the optimal time was 7 days before allografting, while peritransplant and immediate post-transplant intrathymic inoculation of donor T cells was relatively ineffective in the induction of unresponsiveness to donor grafts. We also showed that removal of the antigen-containing thymus in the sublethally irradiated recipients with functioning cardiac allografts consistently caused graft rejection if performed earlier than 21 days after heart transplantation; thymectomy after 21 days of organ transplantation did not affect indefinite survival of the grafts. Thus, it appears that the maintenance of peripheral tolerance to the grafts after 21 days of transplantation may be dependent on the presence of a new clone of antigen-specific tolerant host T cells. These results confirm the immunologic privileged position of the thymus in the induction of central and peripheral tolerance, and suggest that pretreatment with intrathymic MHC class I alloantigens is potentially useful in the induction of unresponsiveness to donor vascularized allografts in adult animals and in man.

Animals↗

PubMed1998

Function and survival of renal allografts from the same donor transplanted into kidney-only or kidney-pancreas recipients.

BACKGROUND: The aim of this study was to assess whether kidney-pancreas transplantation (KPT) compromises the prognosis of kidney transplantation (KT). METHODS: This study included 368 paired recipients who received grafts from the same donor (184 KPT/184 KT), i.e., renal grafts with the same pretransplant functional and pathologic characteristics. RESULTS: KPT recipients (KPR) were significantly younger and included fewer African-Americans (22% vs. 6%, P=0.0005) than recipients of kidney alone (KR). During year 1 after transplant surgery, KPR were re-admitted more often than KR (4.2+/-2 vs. 2.8+/-2, P < 0.0001). The number of acute rejections (AR) and the serum creatinine were not significantly different in KR and KPR up to 3 years after transplant. After 44+/-29 months, 13% of KR and 17% of KPR died (NS), and 17% of KR and 16% of KPR lost their kidneys (NS). In KPR, reduced renal graft survival did not correlate with AR (P=0.44), but it correlated with: older donors, younger recipients, elevated serum creatinine at 6 months, pancreas loss, and the number of episodes of acute graft dysfunction evaluated by biopsy (multivariate analysis). By Cox, graft and patient survival were not significantly different in KR and KPR. However, the patient survival of KPR < 40 years of age was lower than that of KR (P=0.02). Renal biopsies (n=165) in 40 paired recipients showed no significant differences in AR, interstitial fibrosis, or vascular pathology. CONCLUSIONS: Renal graft function, structure, and survival are not different in KPR and KR, but the correlates of renal graft survival are different in these two groups of recipients.

Adult↗

PubMed2006

The role of cyclophosphamide and granulocyte colony-stimulation factor in achieving high-level chimerism in allotransplanted limbs.

The establishment of a high-level of chimerism may be the most stable strategy for donor-specific tolerance. The purpose of this study was to evaluate the efficacy of a new protocol using cyclophosphamide (CYP) and granulocyte colony-stimulation factor (G-CSF) to induce high-level chimerism following rat whole-limb allotransplantation. Seventy-three whole-limb allotransplants from LacZ transgenic rats to LEW rats were performed. CYP was injected at day 2, and G-CSF was given from day 0 to 3. Nontreated limb allografts were rejected after 4.2 days. In FK506-treated group for 28 days, the survival time was prolonged to 64 days. In the group treated with CYP/G-CSF, limb allografts were rejected after 5.4 days and 5 of 15 recipients showed acute lethal graft-versus-host disease (GVHD). Polymerase chain reaction (PCR) study showed a high level of chimerism even within 1 week after transplantation. Fourteen of 30 recipients given CYP/G-CSF/FK506 died within 2 weeks. The limb survival was significantly prolonged, however, with three grafts surviving more than 300 days. Seven recipients (24%) showed chronic GVHD. A high-level of chimerism was maintained when limb allografts were not rejected by recipients. Limb allografting could function as a vascularized carrier for bone marrow transplantation, provide a continuous source of donor cells and contribute to a high level of chimerism in the recipient. Pretransplant CYP followed by G-CSF and FK506 treatment significantly prolonged the survival of limb allografts but frequently caused chronic GVHD in the recipients.

Animals↗

PubMed1991

Assessment of renal function in type I diabetic patients after kidney, pancreas, or combined kidney-pancreas transplantation.

The long-term kidney function (KF) in the three categories of diabetic type 1 pancreas (P) transplant recipients (simultaneous P and kidney [SPK]; P after K [PAK]; PTx alone [PTA] was studied sequentially over a 2-year period in 62 patients who received a bladder-drained allograft that functioned for at least 1 year. Fifty-three (85%) patients were analyzed at 1 month, 42 (68%) at 1 year, and 16 (26%) at 2 years posttransplant. Comparison of KF was made within each recipient category and between categories. In addition, the KF in the SPK and PAK patients was compared to a matched group of diabetic type 1 recipients of KTx alone (functioning at least 1 year). In the SPK group, KF was stable over time: the mean +/- SD serum creatinine (mg/dl) was 1.5 +/- 0.5 at 1 month, 1.8 +/- 1.0 at 1 year, and 1.7 +/- 0.5 at 2 years. In the PAK category, the pre-PTx serum creatinine value was 1.4 +/- 0.5, and then remained stable after the PTx (1.3 +/- 0.2 at 1 month, 1.3 +/- 0.4 at 1 year, and 1.2 +/- 0.4 at 2 years). In the recipients of a PTA, the values at 1 month (1.1 +/- 0.4), 1 year (1.4 +/- 0.5), and 2 years (1.3 +/- 0.5) were significantly higher (P less than or equal to 0.03) than the pre-PTx value (0.9 +/- 0.2); and results at 1 month and 2 years were lower than those at 1 year, a significant difference compared to the 1-month value (P = 0.01). Comparisons between the categories of PTx recipients demonstrated that the pre-PTx value in the PTA group (0.9 +/- 0.2) was significantly lower (P = 0.01) than in the PAK group (1.4 +/- 0.5). At 1 month the serum creatinine value in the PTA category (1.1 +/- 0.4) was significantly lower (P = 0.02) than in the SPK category (1.5 +/- 0.5), but thereafter (1 and 2 years) the difference was not significant (P greater than 0.1). KF in recipients of KTx alone was similar at each post-Tx time point when compared to the SPK and PAK categories. We concluded that a PTx can be performed in diabetics without a detrimental effect on a simultaneously or a previously transplanted kidney and that a statistically significant, albeit minimal to moderate, initial but not progressive deterioration in native KF occurs in recipients of a PTx alone.

Creatinine↗

PubMed1996

Acute leukaemia following renal transplantation.

Four renal transplant patients on immunosuppressive therapy who presented with acute myeloid leukaemia are described. In two cases, azathioprine may have played an important role as a cofactor in leukaemogenesis. In a third case, the alkylating agent cyclophosphamide may have contributed. All patients were treated for leukaemia with full doses of cytotoxic chemotherapy and, in each case, a functioning renal allograft was preserved throughout the treatment despite attenuation of immunosuppressive therapy. Three patients achieved complete remission. Of the three, one is surviving at 2 years and two expired during the pancytopenic phase of their treatment with no active leukaemia present, and with intact renal function. As increasing expertise in the field of organ transplantation allows patients to survive longer, such patients' exposure to immunosuppressive and potentially leukaemogenic drugs is prolonged. The risk of secondary neoplasia has been previously documented in this population. Two of the four cases reported here suffered from polycystic kidney disease as their underlying condition. While this report suggests that the leukaemias are related to renal transplantation, we cannot rule out an association with the underlying disease which led to the transplant. This report further suggests that the leukaemia that develops in such patients may respond to standard therapy, and that such treatment does not compromise the transplanted kidney.

Acute Disease↗

PubMed1995

The magnetic resonance renogram in renal transplant evaluation using dynamic contrast-enhanced MR imaging.

To assess the role of the dynamic gadolinium DTPA (Gd-DTPA) magnetic resonance (MR) renogram in differentiating various causes of renal allograft dysfunction, contrast-enhanced MR imaging studies were performed in 5 normal renal allografts, 5 patients with acute rejection (AR), and 7 patients with cyclosporine nephrotoxicity. Time-versus-signal intensity (SI) curves were plotted. Normal renal allografts showed a rapid increase and slow decay, with a definite peak in cortical (CX) SI curves (peak mean signal intensity (Amax 338.6 +/- 46.5). The outer medullary (OM) (Amax 306.5 +/- 59) and inner medullary (IM) (Amax 263.4 +/- 47.4) curves did not show a definite peak. The OM curve slowly reached a steady state and caught up with the CX curve. AR episodes were characterized by a blunted uprise and delayed peak of CX (Amax 180 +/- 70.9) and a low-amplitude vascular phase with a slow constant uprise of the inner medullary curve (Amax 120.35 +/- 42.4). The OM signal intensity curve (Amax 150.73 +/- 78) failed to catch up with the CX curve. The maximum amplitude of SI curves in CsA-induced allograft dysfunction were low, with no definite peak, and CX, OM, and IM curves ran parallel to each other with a constant gap. Dynamic Gd-DTPA, MR imaging is a noninvasive technique that shows distinct characteristics in acute rejection, cyclosporine nephrotoxicity, and normally functioning renal allografts.

Adult↗

PubMed2006

[Construction of protein fingerprint signature in serum and its significance for early diagnosis with chronic allograft nephropathy].

OBJECTIVE: To construct protein fingerprints in serum and to early diagnose chronic allograft nephropathy (CAN) using surface enhanced laser ionization/desorption-time of flight-mass spectrometry (SELDI-TOF-MS). METHODS: Serum protein spectra were detected by SELDI-TOF-MS and weak cation exchange (CM10), which were from long-term survival patients with well-functioning kidney allograft (LS) (n = 24) and CAN (n = 15), and then biomarkers were screened through the analysis of database with Biomarker Wizard and Biomarker Pattern softwares. RESULTS: 78 protein peaks of interest were generated in each sample, 18 protein spectra statistically show difference between LS and CAN (P < 0.05), 6 of which (m/z 2476.0, 3078.7, 3190.5, 4076.5, 4506.0, 6178.4) statistically show significant difference (P < 0.01), a single biomarker (m/z 3078.7) differentiated LTS and CAN (P = 0.0001), it was upregulated in the former and downregulated in the latter, its diagnostic sensitivity and specificity were 87.5% and 81.8% respectively. Its cost-effective value is 0.307. CONCLUSION: Establishment of protein fingerprint signature in serum by SELDI-TOF-MS is clinically predictive of CAN.

Adult↗

PubMed2004

Cytomegalovirus infection in heart transplant recipients is associated with impaired endothelial function.

BACKGROUND: Cardiac allograft vasculopathy (CAV) is initiated by allograft endothelial injury. We hypothesized that a major mechanism by which cytomegalovirus (CMV) could contribute to CAV is by dysregulation of the endothelial vasomotor response. METHODS: Coronary endothelial vasomotor function was determined in 183 consecutive patients (24+/-33 months after transplantation), and was correlated with recipient and donor CMV serological status before transplantation and with documented CMV infection episodes (CMVpp65Ag+). Serial endothelial function measurements were performed in a subgroup of 53 transplant recipients (1 month and 12 months after transplantation). The composite endpoint of cardiovascular related events and death during a follow-up of 66+/-41 months was analyzed based on the CMV serological status before transplantation. RESULTS: The medium event-free time for CMV-negative recipients of CMV-positive hearts was 8.1 years compared with 13.3 years for the other groups (P<0.05). Distal epicardial but not microvascular endothelial function was significantly impaired in CMV seronegative recipients of seropositive donor hearts (n=48) compared with all other groups (P<0.01 versus seronegative recipient/seronegative donor; P<0.05 versus seropositive recipient/seronegative donor; P<0.05 versus seropositive recipient/seropositive donor). Distal epicardial endothelial dysfunction was more pronounced in heart transplant recipients with a history of documented CMV infection compared with patients without any documented CMV infection (P<0.01). In a longitudinal subgroup analysis, distal epicardial and microcirculatory endothelial vasomotor response deteriorated significantly in recipients with documented CMV infection (P<0.05 versus baseline) but not in patients without previous CMV infection. CONCLUSIONS: Documented CMV infection episodes in heart transplant recipients are associated with impaired coronary endothelial function. CMV-negative recipients of CMV-positive donor hearts have an impaired distal epicardial endothelial function and an increased incidence of cardiovascular-related events and death during follow-up. CMV infection may contribute to allograft failure by accelerating coronary endothelial dysfunction.

Adult↗

PubMed2001

The prevalence of osteopenia in pediatric renal allograft recipients varies with the method of analysis.

BACKGROUND: Pediatric renal allograft recipients often suffer from osteopenia and the potential for increased fractures. Although modern densitometers are widely available, their use in children is complicated by lack of optimal interpretive criteria. METHODS: We reviewed dual energy X-ray absorptiometry (DEXA) studies in 33 patients with functional renal allografts 4.4 +/- 3.6 years after transplantation. We interpreted our data using three previously described methods of assigning bone mineral density (BMD) Z scores. RESULTS: BMD was directly related to age, height, weight, body surface area, and pubertal status (p < 0.001). Using gender-mixed reference data matched by chronological age, the mean BMD Z score was -0.9 +/- 1.3 vs. 0.4 +/- 1.4 when matched by height-age (p < 0.001). Height-age adjustment particularly increased the BMD Z score of pubertal adolescents. In a subset of 22 patients, gender-matched reference data led to different results from the gender-mixed reference population (mean BMD Z score 0.0 +/- 1.7 vs. -0.8 +/- 1.4, p < 0.001). CONCLUSIONS: The perceived prevalence of osteopenia among pediatric kidney transplant recipients differs using analysis based on chronological age, height-age, or gender-matched reference data. Further studies are necessary to determine the clinical significance of measured bone density in this population.

Absorptiometry, Photon↗

PubMed1993

Pathology of kidney transplant rejection.

In the past year there has been considerable progress in defining the morphologic characteristics of the normally functioning renal allograft in the cyclosporine era. Based on these characteristics and knowledge of clinically validated important changes in rejection, internationally agreed upon standardized terms and criteria have been developed for the histologic diagnosis of acute and chronic rejection and allied conditions. Chronic changes observed in normally functioning grafts at 2 years posttransplantation have been shown to predict the presence of renal functional impairment for 4 years. Important new rejection changes have been identified in the peritubular capillaries. Various alternatives to core biopsy have been explored, but no technique as yet has sufficient sensitivity and specificity for general use in rejection diagnosis. The accurate distinction of chronic rejection from other conditions remains a challenge for the future.

Biopsy, Needle↗

PubMed2000

[Posttransplantation diabetes mellitus].

OBJECTIVE: To study the clinical rules of posttransplantation diabetes mellitus (PTDM). METHODS: 21 patients treated from Dec. 1992 to Sept. 1998 were analysed. RESULTS: The morbidity of PTDM was 16.3% of total patients in the corresponding period. Between the groups of PTDM and NON-PTDM, there was statistical significance in age, kidney function and family diabetic history. It was not related to CSA bottom concentration and acute rejection. In this group 2 cases were complicated by hyperosmolar nonketotic diabetic comas (9.5%) and 11 various infections (52.4%). CONCLUSIONS: PTDM as a secondary diabetes due to antirejection drugs and allograft kidney function may cause serious consequences if it is treated improperly.

Adult↗