Is the Presence of 2 Renal Allograft Arteries Associated with Adverse Outcomes in Live Donor Kidney Transplantation?

OBJECTIVE: Although it was postulated that renal grafts with multiple arteries could lead to unfavorable recipient outcomes, this subject remains controversial. This study aimed to compare the outcomes of recipients receiving renal allografts with a single artery with those receiving renal grafts with two arteries. MATERIALS AND METHODS: Adult patients who received live donor kidney transplantation in our center between January 2020 and October 2021 were included. Data including age, gender, body mass index, renal allograft side, pre-kidney transplantation dialysis status, human leukocyte antigen mismatch number, warm ischemia time, the number of renal allograft arteries (single/double), complications, duration of hospitalization, postoperative creatinine levels, glomerular filtration rates, early graft rejection, graft loss, and mortality were collected. Subsequently, patients who received single-artery renal allografts were compared with those who received double-artery renal allografts. RESULTS: Overall, 139 recipients were included. The mean recipient age was 43.73 ± 13.03 (21-69). While 103 recipients were male, 36 were female. The comparison between the 2 groups revealed that mean ischemia time was significantly longer in the double-artery than in the single-artery group (48.0 vs. 31.2 minutes) (P=.00). In addition, the single-artery group had significantly lower postoperative day 1 and day 30 mean serum creatinine levels. Also, the mean postoperative day 1 glomerular filtration rates were significantly higher in the single-artery group than in the double-artery group. However, the 2 groups were similar concerning the glomerular filtration rates measured at other times. On the other hand, there was no difference between the 2 groups regarding duration of hospitalization, surgical complication, early graft rejection, graft loss, and mortality rates. CONCLUSION: The presence of 2 renal allograft arteries does not have adverse effects on the postoperative parameters of the kidney transplantation recipients, including graft function, duration of hospitalization, surgical complication, early graft rejection, graft loss, and mortality rates.

Mesalazine induced focal segmental glomerulosclerosis in a patient with ulcerative colitis.

Focal segmental glomerulosclerosis (FSGS) and other glomerulonephritis due to the use of 5-aminosalicylic acid derivatives have been reported in the literature. A 38-year-old male who had been using mesalazine for four years because of ulcerative colitis applied to doctor due to swelling in the lower extremities. The patient was diagnosed with nephrotic syndrome (NS). Renal biopsy was performed, and FSGS was diagnosed. Antiproteinuric treatments were initiated with steroid therapy. The patient has been followed with the normal renal function of the after treatment. 5-aminosalicylic acid derivatives affect renal functions at different levels and caused in NS.

Renal Transplantation in High Immunological Risk Patients: A Single-Center Experience.

BACKGROUND: Renal transplantation (RT) in high-risk patients is increasingly performed due to an inadequate organ pool and increased rate of RT after a failed transplantation. Safety and prognosis of RT in such patients with high risk is an ongoing debate. Herein we aimed to present our single-center experience on RT of high-risk patients. METHODS: A total of 89 consecutive RT patients were included into this study in a 10-month period. Patients were divided into 3 groups: the low-risk group (n = 47) with negative panel reactive antibody (PRA), medium-risk group (n = 18) with positive PRA but mean fluorescence intensity (MFI) < 2000, and high-risk group (n = 24) with positive PRA and MFI >2000 or donor specific antibody (DSA) positivity. Groups were compared in terms of demographic features, serum creatinine levels, acute rejection rates, delayed graft function (DGF), and patient or graft loss. RESULTS: Age of the recipients were similar between the groups. Desensitization (7% vs 11% vs 42%, respectively, in low-, medium-, and high-risk groups; P = .001), plasmapheresis (6% vs 11% vs 46%, respectively, P < .001), and rituximab treatments (0% vs 0% vs 25%, respectively, P < .001) were significantly more frequently performed in high-risk patients. Serum creatinine levels at 1 month and 6 months after RT were similar between the groups (P = .43 and P = .71, respectively). Rates of acute rejection (6% vs 6% vs 16%, respectively, P = .52) and DGF (9% vs 11% vs 29%, respectively, P = .15) were similar between the groups. Frequencies of loss of patient or graft were also similar (0% vs 6% vs 4%, P = .15). CONCLUSION: RT may be successfully performed in high-risk patients without an increase in the risk of acute rejection, DGF, or patient/graft loss.

Intrarenal application of N-acetylcysteine for the prevention of contrast medium-induced nephropathy in primary angioplasty.

OBJECTIVE: Contrast medium-induced nephropathy (CIN) is a well-known complication of coronary angiographic procedures, especially in patients treated with primary angioplasty. To prevent CIN, we examined using a local application of N-acetylcysteine (NAC) for the prevention of CIN during primary angioplasty. We hypothesized that a local application of NAC into the renal arteries would provide the benefit of a higher local concentration, lower first-pass metabolism, and faster efficacy. To evaluate the effects of NAC by the intrarenal route, we performed a prospective, randomized clinical study in patients with acute myocardial infarction treated with primary angioplasty. METHODS: Participants were 312 patients with ST-segment elevation myocardial infarction undergoing primary angiography. Eligible patients were randomly assigned to receive intravenous NAC, intrarenal NAC, or placebo. RESULTS: Overall, CIN occurred in 74 (23.7%) of the 312 patients. The rate of CIN was 25% in the intravenous NAC group, 22.9% in the intrarenal NAC group, and 23.2% in the placebo group, with no significant effect seen for either treatment (P=0.64). We did find a significant correlation between CIN and ejection fraction (P=0.05) and baseline renal function (P=0.01). CONCLUSION: Both intrarenal and intravenous applications of NAC failed to show any benefit over placebo in the prevention of CIN. This result shows that NAC application does not have any prophylactic effect, dose dependent or otherwise, on CIN, as previously reported. Our results suggest that more attention should be paid to optimize hemodynamic variables for the prevention of CIN.

Improvement of coronary flow velocity reserve with telmisartan in patients with autosomal-dominant polycystic kidney disease.

OBJECTIVES: Endothelial dysfunction (ED) has been reported in patients with autosomal-dominant polycystic kidney disease (ADPKD). Coronary flow velocity reserve (CFVR) is a noninvasive test showing endothelial function of epicardial coronary arteries and coronary microcirculatory function. The aim of this study was to investigate the effect of the angiotensin receptor blocker, telmisartan, on CFVR in patients with ADPKD. METHODS: Thirteen patients with ADPKD and well-preserved renal function and 22 healthy controls were included in the study. CFVR was measured at baseline and after dipyridamole infusion by echocardiography. CFVR was calculated as the ratio of hyperemic to baseline average peak diastolic velocities. After the baseline evaluation of CFVR, patients started telmisartan at a dose of 80 mg/day and were followed for 12 months. CFVR was remeasured after 6 and 12 months of therapy. RESULTS: Patients with ADPKD had significantly lower CFVR compared to healthy subjects. CFVR increased significantly after 6 months and 12 months of telmisartan therapy (P = 0.001) in patients with ADPKD. CONCLUSION: One year of telmisartan therapy significantly improved CFVR in patients with ADPKD. This finding suggests that the stimulation of the renin-angiotensin-aldosterone system contributes to the ED in these patients.

Coronary flow velocity reserve and carotid intima media thickness in patients with autosomal dominant polycystic kidney disease: from impaired tubules to impaired carotid and coronary arteries.

BACKGROUND AND OBJECTIVES: Cardiovascular problems are a major cause of morbidity and mortality in patients with autosomal dominant polycystic kidney disease. Endothelial dysfunction, an early and reversible feature in the pathogenesis of atherosclerosis, is associated with increased vascular smooth muscle tone, arterial stiffening, and increased intima-media thickness. Coronary flow velocity reserve is a noninvasive test showing endothelial function of epicardial coronary arteries and coronary microcirculatory function. The aim of the study was to investigate the carotid intima-media thickness and coronary flow velocity reserve in patients with autosomal dominant polycystic kidney disease. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Thirty normotensive patients with autosomal dominant polycystic kidney disease (10 male, 20 female) with well-preserved renal function and 30 healthy subjects (12 male, 18 female) were included in the study. Coronary flow velocity reserve was measured at baseline and after dipyridamole infusion by echocardiography. Coronary flow velocity reserve was calculated as the ratio of hyperemic to baseline diastolic peak velocities. RESULTS: Carotid intima-media thickness was significantly higher in patients than in control subjects (0.80 +/- 0.29 versus 0.54 +/- 0.14 mm, respectively; P < 0.001). Moreover, coronary flow velocity reserve was significantly lower in patients than in control subjects (1.84 +/- 0.39 versus 2.65 +/- 0.68, respectively; P < 0.001). CONCLUSIONS: Normotensive patients with autosomal dominant polycystic kidney disease with well-preserved renal function have significantly increased carotid intima-media thickness and significantly decreased coronary flow velocity reserve compared with healthy subjects. These findings suggest that atherosclerosis starts at an early stage in the course of their disease in patients with autosomal dominant polycystic kidney disease.

An unusual patient with hypercalciuria, recurrent nephrolithiasis, hypomagnesemia and G227R mutation of Paracellin-1. An unusual patient with hypercalciuria and hypomagnesemia unresponsive to thiazide diuretics.

A 19-year-old female patient with hypercalciuria and recurrent nephrolithiasis/urinary tract infection unresponsive to thiazide type diuretics is presented. The patient first experienced nephrolithiasis at the age of 4 years. Afterwards, recurrent passages of stones and urinary tract infection occurred. On diagnostic evaluation at the age of 19 years, she also had hypocitraturia and hypomagnesemia. Her serum calcium concentrations were near the lower limit of normal (8.5-8.8 mg/dl; normal range: 8.5-10.5), her serum magnesium concentrations were 1.15-1.24 mg/dl (normal range: 1.4-2.5) and urinary calcium excretion was 900 mg/24 h. PTH concentrations were increased (110-156 pg/ml; normal range: 10-65). We tried to treat the patient with hydrochlorothiazide at a dose of 50 mg/day. During treatment with thiazide diuretics, PTH concentration remained high and the patient had recurrent urinary tract infections and passages of stones. Serum magnesium concentration did not normalize even under the parenteral magnesium infusion. Her mother had a history of nephrolithiasis 20 years ago. Severe hypomagnesemia in association with hypercalciuria/urinary stones is reported as a rare autosomal recessive disorder caused by impaired reabsorption of magnesium and calcium in the thick assending limp of Henle's loop. Recent studies showed that mutations in the CLDN16 gene encoding paracellin-1 cause the disorder. In exon 4, a homozygous nucleotide exchange (G679C) was identified for the patient. This results in a point mutation at position Glycine227, which is replaced by an Arginine residue (G227R). The mother was heterozygous for this mutation. G227 is located in the fourth transmembrane domain and is highly conserved in the claudin gene family. This case indicates the pathogenetic role of paracellin-1 mutation in familial hypomagnesemia with hypercalciuria and nephrocalcinosis and further underlines the risk of stone formation in heterozygous mutation carriers.