Role of Prior Split Renal Function for Living Kidney Transplantation in Recipients and Donors

Introduction and objectives: Congenital ureteropelvic junction obstruction (UPJO) is the most common cause of hydronephrosis. Management protocols are based on the presence of symptoms and when the patient is asymptomatic the function of the affected kidney determines the line of treatment. Percutaneous nephrostomy (PCN) became a widely accepted procedure in children in the 1990s. The aim of the study was to evaluate the results of performing percutaneous nephrostomy (PCN) in all patients with UPJO and split renal function (SRF) of less than 10% in the affected kidney, because the management of such cases is still under debate. Methods:This prospective clinical trial was carried out at Dhaka Medical College Hospital from January 2014 to December 2016. Eighteen consecutive patients who underwent PCN for the treatment of unilateral UPJO were evaluated prospectively. In these children, ultrasonography was used for puncture and catheter insertion. Local anesthesia with sedation or general anesthesia was used for puncture. Pig tail catheters were employed. The PCN remained in situ for at least 4 weeks, during which patients received low-dose cephalosporin prophylaxis. Repeat renography was done after 4 weeks. When there was no significant improvement in split renal function (10% or greater) and PCN drainage (greater than 200 ml per day) then nephrectomies were performed otherwise pyeloplasties were performed. The patients were followed up after pyeloplasty with renograms at 3 months and 6 months post operatively. Results: All the patients had severe hydronephrosis during diagnosis and 14 patients with unilateral UPJO were improved after PCN drainage and underwent pyeloplasty. The rest four patients that did not show improvement in the SRF and total volume of urine output underwent nephrectomy. In the patients with unilateral UPJO who improved after PCN drainage, the SRF was increased to 26.4% ±8.6% (mean± SD) after four weeks and pyeloplasty was performed. At three and six months follow-up, SRF value was 29.2% ±8.5% and 30.8.2% ±8.8% respectively. Conclusion: Before planning of nephrectomy in poorly functioning kidneys (SRF < 10%) due to congenital UPJO, PCN drainage should be done to asses improvement of renal function. Bangladesh Journal of Urology, Vol. 20, No. 2, July 2017 p.61-64

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The Emerging Role of DNA Methylation in Kidney Transplantation: A Perspective

American Journal of Transplantation ◽

10.1111/ajt.13585 ◽

2016 ◽

Vol 16 (4) ◽

pp. 1070-1078 ◽

Cited By ~ 8

Author(s):

L. Heylen ◽

B. Thienpont ◽

M. Naesens ◽

D. Lambrechts ◽

B. Sprangers

Keyword(s):

Dna Methylation ◽

Kidney Transplantation

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Neuronal regulation of renal function: A model system for nervous system interactions

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y92-097 ◽

1992 ◽

Vol 70 (5) ◽

pp. 733-734 ◽

Cited By ~ 1

Author(s):

J. Michael Wyss

Keyword(s):

Nervous System ◽

Renal Function ◽

Renal Disease ◽

Easy Access ◽

Renal Nerves ◽

Clinical Consequence ◽

Nerve Activity ◽

Renal Nerve ◽

Renal Nerve Activity

The kidney is the most highly innervated peripheral organ, and both the excretory and endocrine functions of the kidney are regulated by renal nerve activity. The kidney plays a dominant role in body fluid homeostasis, blood ionic concentration, and pH and thereby contributes importantly to systemic blood pressure control. Early studies suggested that the neural-renal interactions were responsible only for short-term adjustments in renal function, but more recent studies indicate that the renal nerves may be a major contributor to chronic renal defects leading to established hypertension and (or) renal disease. The neural-renal interaction is also of considerable interest as a model to elucidate the interplay between the nervous system and peripheral organs, since there is abundant anatomical and physiological information characterizing the renal nerves. The investigator has easy access to the renal nerves and the neural influence on renal function is directly quantifiable both in vivo and in vitro. In this symposium that was presented at the 1990 annual convention of the Society for Neuroscience in St. Louis, Missouri, three prominent researchers evaluate the most recent progress in understanding the interplay between the nervous system and the kidney and explore how the results of these studies relate to the broader questions concerning the nervous system's interactions.First, Luciano Barajas examines the detailed anatomy of the intrarenal distribution of the efferent and afferent renal nerves along the nephron and vasculature, and he evaluates the physiological role of each of the discrete components of the innervation. His basic science orientation combined with his deep appreciation of the clinical consequence of the failure of neural-renal regulation enhances his discussion of the anatomy. Ulla C. Kopp discusses the role of the renorenal reflex, which alters renal responses following stimulation of the contralateral kidney. She also considers her recent findings that efferent renal nerve activity can directly modify sensory feedback to the spinal cord from the kidney. Finally, J. Michael Wyss examines the functional consequences of neural control of the kidney in health and disease. Although the nervous system has often been considered as only an acute regulator of visceral function, current studies into hypertension and renal disease suggest that neural-renal dysfunction may be an important contributor to chronic diseases.Together, these presentations examine most of the recent advances in the area of neural-renal interactions and point out how these data form a basis for future research into neuronal interactions with all visceral organs. The relative simplicity of the neural-renal interaction makes this system an important model with which to elucidate all neural-peripheral and neural-neural interactions.

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A Kidney Transplant Recipient with Recurrent Henoch-Schönlein Purpura Nephritis Successfully Treated with Steroid Pulse Therapy and Epipharyngeal Abrasive Therapy

Nephron ◽

10.1159/000511166 ◽

2020 ◽

pp. 1-5

Author(s):

Mika Fujimoto ◽

Kan Katayama ◽

Kouhei Nishikawa ◽

Shoko Mizoguchi ◽

Keiko Oda ◽

...

Keyword(s):

Renal Function ◽

Kidney Transplantation ◽

Transplant Recipient ◽

Kidney Transplant ◽

Kidney Transplant Recipient ◽

Pulse Therapy ◽

Steroid Pulse Therapy ◽

Steroid Pulse ◽

Schonlein Purpura ◽

Purpura Nephritis

There is no specific treatment for recurrent Henoch-Schönlein purpura nephritis (HSPN) in a transplanted kidney. We herein report a case of a kidney transplant recipient with recurrent HSPN that was successfully treated with steroid pulse therapy and epipharyngeal abrasive therapy (EAT). A 39-year-old Japanese man developed HSPN 4 years ago and had to start hemodialysis after 2 months despite receiving steroid pulse therapy followed by oral prednisolone, plasma exchange therapy, and cyclophosphamide pulse therapy. He had undergone tonsillectomy 3 years earlier in the hopes of achieving a better outcome of a planned kidney transplantation and received a living-donor kidney transplantation from his mother 1 year earlier. Although there were no abnormalities in the renal function or urinalysis 2 months after transplantation, a routine kidney allograft biopsy revealed evidence of mesangial proliferation and cellular crescent formation. Mesangial deposition for IgA and C3 was noted, and he was diagnosed with recurrent HSPN histologically. Since the renal function and urinalysis findings deteriorated 5 months after transplantation, 2 courses of steroid pulse therapy were performed but were ineffective. EAT using 0.5% zinc chloride solution once per day was combined with the third course of steroid pulse therapy, as there were signs of chronic epipharyngitis. His renal function recovered 3 months after daily EAT and has been stable for 1.5 years since transplantation. Daily EAT continued for >3 months might be a suitable strategy for treating recurrent HSPN in cases of kidney transplantation.

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P0523PROTECTIVE ROLE OF REGULATORY B CELLS ON THE RENAL TISSUE REPAIRMEN AFTER ISCHEMIA REPERCUSSION INJURY

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa142.p0523 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

Yokota Yunosuke ◽

Goh Kodama ◽

Sakuya Itou ◽

Yosuke Nakayama ◽

Nobukazu Komatsu ◽

...

Keyword(s):

Flow Cytometry ◽

Renal Function ◽

B Cells ◽

Interleukin 10 ◽

Renal Tissue ◽

Protective Role ◽

Regulatory B Cells ◽

Tubulointerstitial Injury ◽

Iri Model

Abstract Background and Aims Acute kidney injury (AKI), even if followed by renal recovery, is a risk factor for the future development of chronic kidney disease (CKD) and end- stage renal disease. It has been postulated that interleukin-10 (IL-10)-producing Regulatory B cells (Breg) play an important role for the tissue repairment in several tissues and organs. Basically, protective role of Breg has been reported in inflammatory bowel disease. In the kidney, it has been shown that IL-10 suppresses renal function decline and improves renal prognosis in IRI model, a typical model of AKI. However, the identity of Breg in the kidney and their origin have not been clarified. Further, how the Breg works during the transition from AKI to CKD is not known. Therefore, first we investigated whether Breg existed in renal tissue on the progression from AKI to CKD in IRI model mice. Further, we performed splenectomy, and examined the renal injury, Breg, and plasma IL-10 levels in this model. Method To examine the existence of Breg in the kidney of IRI model, we used 8-10 weeks-old GFP / IL-10 mice based on C57BL / 6J mice. They are reporter mice for IL-10 producing cells, and can visualize IL-10 producing cells under a fluorescence microscope without fluorescent immunostaining. We prepared following three groups, sham, IRI (unilateral), and IRI + SN (splenectomy) groups. Mice were anesthetized with chloral hydrate (4 g/kg,, intraperitoneal). After making a midline incision, exposed a blood vessel of the left renal pedicles and clamped it for 30 min by clips. one day, 7 days, and 14 days after the surgery, mice were sacrificed, and renal function and plasma IL-10 levels as well as tissue damages by PAS and Masson’s Trichrome staining were assessed. Tissue IL-10-producing cells were detected by flow cytometry. Results There was no difference of plasma IL-10 levels and renal tubulointerstitial injury in IRI group and IRI+SN group on day 1 after IRI. However, on day 7 and day 14, plasma IL-10 levels became gradually higher in IRI group, and SN decreased the increase in IL-10 levels. Tubulointerstitial injury was induced by IRI and SN further worsened tubular damages. Serum Cr and BUN levels were not different in three groups due to normal right kidney. On day 1, number of IL-10-producing B cells increased in the spleen and renal medulla in IRI group confirmed by flow cytometry, which was completely diminished by SN, suggesting that origin of the infiltrated Breg might be spleen, thereby being involved in the protective role in IRI injury in the kidney. Conclusion We report for the first time that Breg might be recruited from spleen by AKI, which may be one of the mechanisms to prevent the progression to CKD.

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Metabolic Syndrome and Salt-Sensitive Hypertension in Polygenic Obese TALLYHO/JngJ Mice: Role of Na/K-ATPase Signaling

International Journal of Molecular Sciences ◽

10.3390/ijms20143495 ◽

2019 ◽

Vol 20 (14) ◽

pp. 3495 ◽

Cited By ~ 1

Author(s):

Yanling Yan ◽

Jiayan Wang ◽

Muhammad A. Chaudhry ◽

Ying Nie ◽

Shuyan Sun ◽

...

Keyword(s):

Blood Pressure ◽

Renal Function ◽

Significant Rise ◽

Protein Carbonylation ◽

High Salt ◽

Kidney Cortex ◽

High Salt Diet ◽

Salt Diet ◽

Salt Sensitive Hypertension

We have demonstrated that Na/K-ATPase acts as a receptor for reactive oxygen species (ROS), regulating renal Na+ handling and blood pressure. TALLYHO/JngJ (TH) mice are believed to mimic the state of obesity in humans with a polygenic background of type 2 diabetes. This present work is to investigate the role of Na/K-ATPase signaling in TH mice, focusing on susceptibility to hypertension due to chronic excess salt ingestion. Age-matched male TH and the control C57BL/6J (B6) mice were fed either normal diet or high salt diet (HS: 2, 4, and 8% NaCl) to construct the renal function curve. Na/K-ATPase signaling including c-Src and ERK1/2 phosphorylation, as well as protein carbonylation (a commonly used marker for enhanced ROS production), were assessed in the kidney cortex tissues by Western blot. Urinary and plasma Na+ levels were measured by flame photometry. When compared to B6 mice, TH mice developed salt-sensitive hypertension and responded to a high salt diet with a significant rise in systolic blood pressure indicative of a blunted pressure-natriuresis relationship. These findings were evidenced by a decrease in total and fractional Na+ excretion and a right-shifted renal function curve with a reduced slope. This salt-sensitive hypertension correlated with changes in the Na/K-ATPase signaling. Specifically, Na/K-ATPase signaling was not able to be stimulated by HS due to the activated baseline protein carbonylation, phosphorylation of c-Src and ERK1/2. These findings support the emerging view that Na/K-ATPase signaling contributes to metabolic disease and suggest that malfunction of the Na/K-ATPase signaling may promote the development of salt-sensitive hypertension in obesity. The increased basal level of renal Na/K-ATPase-dependent redox signaling may be responsible for the development of salt-sensitive hypertension in polygenic obese TH mice.

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