Kidney transplantation from living donor with monolateral renal artery fibromuscular dysplasia using a cryopreserved iliac graft for arterial reconstruction: a case report and review of the literature.

BACKGROUND: Aging and mortality of patients on waiting lists for kidney transplantation have increased, as a result of the shortage of organs available all over the world. Living donor grafts represent a significant source to maintain the donor pool, and resorting successfully to allografts with arterial disease has become a necessity. The incidence of renal artery fibromuscular dysplasia (FMD) in potential living renal donors is reported to be 2-6%, and up to 4% of them present concurrent extra-renal involvement. CASE PRESENTATION: We present a case of renal transplantation using a kidney from a living donor with monolateral FMD. Resection of the affected arterial segment and its subsequent replacement with a cryopreserved iliac artery graft from a deceased donor were performed. No intraoperative nor post-operative complications were reported. The allograft function promptly resumed, with satisfying creatinine clearance, and adequate patency of the vascular anastomoses was detected by Doppler ultrasounds. CONCLUSION: Literature lacks clear guidelines on the eligibility of potential living renal donors with asymptomatic FMD. Preliminary assessment of the FMD living donor should always rule out any extra-renal involvement. Whenever possible, resection and reconstruction of the affected arterial segment should be taken into consideration as this condition may progress after implantation.

A pseudo-three-dimensional model for quantification of oxygen diffusion from preglomerular arteries to renal tissue and renal venous blood.

To assess the physiological significance of arterial-to-venous (AV) oxygen shunting, we generated a new pseudo-three-dimensional computational model of oxygen diffusion from intrarenal arteries to cortical tissue and veins. The model combines the 11 branching levels (known as "Strahler" orders) of the preglomerular renal vasculature in the rat, with an analysis of an extensive data set obtained using light microscopy to estimate oxygen mass transfer coefficients for each Strahler order. Furthermore, the AV shunting model is now set within a global oxygen transport model that includes transport from arteries, glomeruli, peritubular capillaries, and veins to tissue. While a number of lines of evidence suggest AV shunting is significant, most importantly, our AV oxygen shunting model predicts AV shunting is small under normal physiological conditions (~0.9% of total renal oxygen delivery; range 0.4-1.4%), but increases during renal ischemia, glomerular hyperfiltration (~2.1% of total renal oxygen delivery; range 0.84-3.36%), and some cardiovascular disease states (~3.0% of total renal oxygen delivery; range 1.2-4.8%). Under normal physiological conditions, blood Po2 is predicted to fall by ~16 mmHg from the root of the renal artery to glomerular entry, with AV oxygen shunting contributing ~40% and oxygen diffusion from arteries to tissue contributing ~60% of this decline. Arterial Po2 is predicted to fall most rapidly from Strahler order 4, under normal physiological conditions. We conclude that AV oxygen shunting normally has only a small impact on renal oxygenation, but may exacerbate renal hypoxia during renal ischemia, hyperfiltration, and some cardiovascular disease states.

Unwrapping the origins and roles of the renal endothelium.

The renal vasculature, like all vessels, is lined by a thin layer of simple squamous epithelial cells called an endothelium. These endothelial-lined vessels can be subdivided into four major compartments: arteries, veins, capillaries and lymphatics. The renal vasculature is a highly integrated network that forms through the active processes of angiogenesis and vasculogenesis. Determination of the precise contribution of these two processes and of the molecular signaling that governs the differentiation, specification and maturation of these critical cell populations is the focus of an actively evolving field of research. Although much of the focus has concentrated on the origin of the glomerular capillaries, in this review we extend the investigation to the origins of the endothelial cells throughout the entire kidney and the signaling events that cause their distinct functional and molecular profiles. A thorough understanding of endothelial cell biology may play a critical role in a better understanding of renal vascular diseases.

Transvenous stimulation of the renal sympathetic nerves increases systemic blood pressure: a potential new treatment option for neurocardiogenic syncope.

BACKGROUND: Neurocardiogenic syncope (NCS) is a common and sometimes debilitating disorder, with no consistently effective treatment. NCS is due to a combination of bradycardia and vasodilation leading to syncope. Although pacemaker devices have been tried in treating the bradycardic aspect of NCS, no device-based therapy exists to treat the coexistent vasodilation that occurs. The renal sympathetic innervation has been the target of denervation to treat hypertension. We hypothesized that stimulation of the renal sympathetic nerves can increase blood pressure and counteract vasodilation in NCS. METHODS AND RESULTS: High-frequency stimulation (800-900 pps, 10 V, 30-200 seconds) was performed using a quadripolar catheter in the renal vein of 7 dogs and 1 baboon. A significant increase in blood pressure (BP; mean [SD] systolic BP 117 [±28] vs. 128 [±33], diastolic BP 75 [±19] vs. 87 [±29] mmHg) was noted during the stimulation, which returned to baseline after cessation of stimulation. The mean increase in systolic and diastolic BP was 13.0 (±3.3) (P = 0.006) and 10.2 (±4.6) (P = 0.08), respectively. CONCLUSION: We report the first ever study of feasibility and safety of high-frequency electrical stimulation of the renal sympathetic innervation to increase BP in animal models. This has potential applications in the treatment of hypotensive states such as NCS.

Renal vein cytokine release as an index of renal parenchymal inflammation in chronic experimental renal artery stenosis.

BACKGROUND: Renal parenchymal inflammation is a critical determinant of kidney injury in renal artery stenosis (RAS) but is difficult to assess in the single kidney without tissue samples. Whether renal vein (RV) levels of inflammatory markers reflect active parenchymal inflammation remains unknown. We evaluated the relationship between net RV cytokine release and tissue inflammation in the post-stenotic kidney. METHODS: Pigs were studied after 10 weeks of RAS treated 4 weeks earlier with intra-renal vehicle or anti-inflammatory mesenchymal stem cells (MSCs) or normal control. Single-kidney renal blood flow was measured by fast computerized tomography. RV and inferior vena cava levels of tumor necrosis factor (TNF)-α, interferon (IF)-γ, monocyte chemoattractant protein (MCP-1) and interleukin (IL)-10 were measured by enzyme-linked immunosorbent assay, and their net release calculated. Renal expression of the same cytokines was correlated with their net release. RESULTS: Net release of TNF-α, IF-γ and MCP-1 was higher in RAS compared with normal and to the contralateral kidney (all P<0.05), decreased in MSC-treated pigs as was their tissue expression. Contrarily, the release of the anti-inflammatory IL-10 was lower in RAS and normalized in RAS+MSC. The net release of TNF-α, MCP-1 and IL-10 directly correlated with their tissue expression. The ratio of inflammatory-to-reparative macrophages directly correlated with the release of MCP-1, but inversely with the release of IL-10. In vitro cultured MSCs also induced a shift in the macrophage phenotype from inflammatory (M1) to reparative (M2). CONCLUSIONS: Our findings demonstrate that the release of inflammatory markers from the affected kidney provides an index of renal tissue inflammation in experimental RAS.

Analysis of retinal circulation using an image-based network model of retinal vasculature.

This paper presents the results of a circulation analysis using an image based network model of a murine retinal vasculature, which closely represents the 3D vascular distribution of the retina. The uneven distribution of the red blood cells at vascular network bifurcations (i.e., plasma skimming effect), the microvascular diameter effect (i.e., Fahraeus-Lindqvist effect) and the role of endothelium surface layer (i.e., in vivo viscosity) were considered in determining the viscosity of the blood in the retinal vessel segments. The study yielded detailed distributions of the hemodynamic quantities in the arterial and venous trees shown in various anatomical based contour plots. Quantitative analysis was also carried out based on statistical distributions. The analysis shows that the distribution of the blood hematocrit (H(D)) in the retinal network is very non-uniform, with lower values at the pre-equator region (near the optic disc) and higher values in the equator region of the retina. This has significant influence on the distribution of apparent viscosity, pressure and wall shear stress (WSS) in the vasculature. The viscosity is generally higher in smaller vessels (i.e., pre-capillary vessels) but exceptions occur in some vessels where the H(D) is small. WSS is greater in smaller vessels located near the optic disc than that in the mainstream retinal vessels. The results presented can be directly useful to ophthalmologists and researchers working with retinal vasculature.

Toward an optimal position for inferior vena cava filters: computational modeling of the impact of renal vein inflow with Celect and TrapEase filters.

PURPOSE: To evaluate the hemodynamic effects of renal vein inflow and filter position on unoccluded and partially occluded inferior vena cava (IVC) filters with use of three-dimensional computational fluid dynamics. MATERIALS AND METHODS: Three-dimensional models of the TrapEase and Günther Celect IVC filters, spherical thrombi, and an IVC with renal veins were constructed. Hemodynamics of steady-state flow was examined for unoccluded and partially occluded TrapEase and Günther Celect IVC filters in varying proximity to the renal veins. RESULTS: Flow past the unoccluded filters demonstrated minimal disruption. Natural regions of stagnant/recirculating flow in the IVC were observed superior to the bilateral renal vein inflows. High flow velocities and elevated shear stresses were observed in the vicinity of renal inflow. Spherical thrombi induce stagnant/recirculating flow downstream of the thrombus. Placement of the TrapEase filter in the suprarenal position resulted in a large area of low shear stress/stagnant flow within the filter just downstream of thrombus trapped in the upstream trapping position. CONCLUSIONS: Filter position with respect to renal vein inflow influences filter trapping hemodynamics. Placement of the TrapEase filter in a suprarenal location may be thrombogenic, with redundant areas of stagnant/recirculating flow and low shear stress along the caval wall caused by the upstream trapping position and the naturally occurring region of stagnant flow from the renal veins. Infrarenal vein placement of IVC filters in a near-juxtarenal position with the downstream cone near the renal vein inflow likely confers increased levels of mechanical lysis of trapped thrombi from increased shear stress from renal vein inflow.

Venous blood flow in maternal kidneys in third trimester of pregnancy.

Objectives: Maternal intra-abdominal pressure and hemodynamics change during pregnancy. The left renal vein may be compressed between the uterus and the spine and aorta, causing congestion and impaired venous return from the left kidney during late pregnancy. The aim of this study was to compare venous and arterial blood flow between the right and left kidney in the third trimester in women without known pregnancy complications.Methods: We conducted a prospective cohort study in 50 women with uncomplicated third-trimester pregnancies at Trondheim University Hospital, Norway, from January to April 2018. The arterial and venous blood flow were examined with pulsed wave Doppler in the hilum of the kidneys and the cross section of the area (CSA) of the vessels was measured from 3D acquisitions. Two diameters of the main vein and artery were measured after rotating the image of the vessels in the C-plane to be as circular as possible. CSA was calculated as π×(mean diameter/2)2. Blood flow volume (ml/minute) in the vessels were calculated as 0.5 × TAmax (cm/s)×CSA (cm2)×60. The main outcome was venous and arterial blood flow volumes, and secondary outcomes were maximum velocity (Vmax), minimum velocity (Vmin), pulsatile index (PI), time-averaged maximum flow (TAmax) and renal interolobar vein impedance index (RIVI). We also examined possible associations between blood flow and maternal age, BMI and blood pressure.Results: We observed differences in venous flow parameters between the two kidneys. The mean total flow volume in the renal veins was 274 ml/min in the left vein versus 358 ml/min in the right vein (p=.10). Vmax, TAmax, PI, and RIVI were all significantly lower in the left renal vein. No differences in arterial blood flow between the two kidneys were found. BMI was negatively correlated to flow in the left renal vein (r= -0.28; p<.05), but not associated to flow in the right renal vein.Conclusion: We found that venous flow pattern differs between left and right renal veins in uncomplicated late pregnancies, but the total flow was not significantly different. New studies should be done in women with preeclampsia.

Circulating adhesion molecules and purine nucleotides during kidney allograft reperfusion.

The impairment of organ function due to ischemia-reperfusion injury is still an important problem in solid organ transplantation. Numerous experimental and clinical studies of native organs have shown that ischemia-reperfusion constitutes an acute inflammatory process involving cell surface adhesion molecule expression. These markers are crucial for the recruitment and infiltration of effector cells into the postischemic tissue. Purines released by the postischemic tissue as the products of the degradation of high-energy nucleotides can be regarded as markers of disturbed energy metabolism. The aim of this study was to examine the correlation between circulating adhesion molecules and purine metabolites in graft renal vein plasma during 49 cases of kidney reperfusion. E-selectin, ICAM-1, and VCAM-1 concentrations correlated positively with hypoxanthine concentrations during reperfusion, whereas the concentrations of ICAM-1 correlated negatively with xanthine concentrations. The results of the present study suggested that the concentrations of adhesion molecules in the renal vein during reperfusion correlated with purine metabolites, reflecting metabolic changes in renal tissue.

Anesthetic management of radical nephrectomy in patients with renal cell carcinoma involving renal vein or inferior vena cava.

OBJECTIVE: To investigate the perioperative anesthetic management of patients diagnosed with renal cell carcinoma (RCC) metastasized into the renal vein or inferior vena cava (IVC) after undergoing radical nephrectomy to provide clinical evidence for rational anesthetic interventions. METHODS: A total of 81 patients with RCC extending into the renal vein or IVC, aged 17-73 years, undergoing radical nephrectomy were recruited. Preoperative status, intraoperative management, average operation time, average estimated blood loss, postanesthesia outcomes, and postoperative complications were retrospectively analyzed. RESULTS: The mean operation time was 288 minutes (range 146-825 minutes). The mean estimated blood loss was recorded as 1905 mL (range 200-7000 mL). Among 81 cases, 9 patients (11.1%, 1 level II, 3 level III, and 5 level IV) were switched to undergo cardiopulmonary bypass. Significant hemodynamic fluctuations were observed in 39 patients who presented with level II-IV of tumor thrombus. One patient had pulmonary embolism and died of active cardiopulmonary resuscitation. The mean postoperative hospital stay was 12.8 days. Twenty-five cases with level III-IV tumor thrombus were transferred to the intensive care unit with endotracheal intubation due to massive intraoperative blood loss. The remaining 55 cases were transferred to the postanesthesia care unit 2 hours before being transferred to the ward. One patient had postoperative acute coronary syndrome and was discharged after effective interventions. CONCLUSION: Anesthetic management and intensive postoperative care play a pivotal role in the success of complete resection of RCC that metastasize into the IVC.

L-arginine metabolism in dog kidney and isolated nephron segments.

The renal basic amino acid metabolism often differs in rodents, strict carnivores, and omnivore species. Given the pivotal role of L-arginine and L-ornithine in several metabolic pathways and the fact that the dog is closely related to humans, being also an omnivore, we tested whether L-arginine metabolism and L-ornithine catabolism take place in the dog kidney. We examined the metabolism of L-arginine in dog cortical tubules to integrate local L-arginine metabolism into a general physiological and metabolic framework. To achieve these goals, we first ascertained the protein expression of relevant enzymes by Western blot. L-Arginine catabolism was studied in suspensions of canine cortical proximal tubules, medullary thick ascending limbs, and papillary collecting ducts either incubated without exogenous L-arginine being added (small endogenous quantities) or incubated with L-arginine being added in supraphysiological amounts (2 mmol/L with or without the presence of alternative metabolic substrates, 2 mmol/L L-glutamine, or lactate). The results revealed that dog kidneys consumed L-citrulline and released L-arginine and L-ornithine. Argininosuccinate synthetase and lyase, arginase II, and ornithine aminotransferase were detected in the renal cortex. Arginase II activity was found in a suspension of proximal tubules by measuring the amounts of urea and L-ornithine produced. A fraction of this L-ornithine was further partially metabolized through the intramitochondrial ornithine aminotransferase pathway, leading to changes in L-glutamate, glucose, L-alanine, and ammonia metabolism without L-proline accumulation. Medullary thick ascending limbs expressed a very low arginase activity, whereas papillary collecting ducts did not. In conclusion, the dog kidney produces L-arginine. Part of this L-arginine is further catabolized by arginase II, suggesting that its physiological role was to produce L-ornithine for the body.

A microperfusion study of sucrose movement across the rat proximal tubule during renal vein constriction.

Constriction of the renal vein has been shown to inhibit net sodium and water reabsorption by the rat proximal tubule. The mechanism is unknown but might be the result of inhibition of the active sodium pump induced by changes in the interstitial fluid compartment of the kidney, or to enhanced passive backflux of sodium and water into the cell or directly into the tubular lumen. Since passive movement of solutes across epithelial membranes is determined in part by the permeability characteristics of the epithelium, an increase in the permeability of the proximal tubule during venous constriction would suggest that enhanced passive flux is involved in the inhibition of reabsorption. In the present experiments, isolated segments of rat proximal convoluted tubules were microperfused in vivo with saline while the animals were receiving (14)C-labeled sucrose intravenously. In normal control animals, no sucrose was detected in the majority of the collected tubular perfusates. In rats with renal vein constriction (RVC), however, sucrose consistently appeared in the tubular perfusates. The rate of inflow of sucrose correlated with the length of the perfused segment, estimated by fractional water reabsorption. In another group of animals with renal vein constriction, inulin-(14)C was given intravenously and the proximal tubules similarly microperfused. Inulin did not appear in the majority of collected perfusates in these animals. These observations indicate that a physiological alteration in the permeability of the proximal tubule occurs during RVC. Such an increase in permeability is consistent with the view that enhanced passive extracellular back-flux plays a role in the reduction of net sodium and water reabsorption in this experimental condition.

Renal tubular permeability during increased intrarenal pressure.

Renal tubular permeability was studied by microinjection techniques during increased intrarenal pressure in anesthetized diuretic rats. Intrarenal pressure, as evidenced by intratubular pressure (ITP), was increased by elevation of ureteral pressure, partial renal venous constriction, or massive saline diuresis. Various combinations of radioactive inulin, creatinine, mannitol, sucrose, and iothalamate in isotonic saline were microinjected into superficial proximal and distal convolutions, and recovery of the isotopes was measured in the urine. Inulin was completely recovered in the urine from the injected kidney at both normal and elevated ITP. Creatinine, mannitol, sucrose, and iothalamate were also completely recovered at normal ITP, but recoveries were significantly lower, averaging 73, 85, 89, and 85%, respectively, after early proximal injection when proximal ITP was increased to 30+/-2 mm Hg by elevation of ureteral pressure. Since transit time is prolonged under these conditions, mannitol recovery was also studied during aortic constriction, which prolongs transit time but lowers ITP. Recovery was complete. A significant loss of mannitol was observed during massive saline diuresis, which shortens transit time but increases ITP. During renal venous constriction producing a proximal ITP of 30+/-2 mm Hg, mannitol recovery was significantly less than 100% even after microinjection into distal convolutions, but the loss was greater injection at more proximal puncture sites. Mannitol recovery was complete during elevation of ureteral pressure in the contralateral kidney. These studies demonstrate a change in the permeability characteristics of all major segments of the renal tubule during elevation of intrarenal pressure. This change is rapidly reversible and does not appear to be due to a humoral factor which gains access to the general circulation.

Mechanism of effect of thoracic inferior vena cava constriction on renal water excretion.

Persistent secretion of vasopressin and/ or diminished distal fluid delivery have been proposed to explain the impaired water excretion associated with low-output cardiac failure. In the present investigation cardiac output (CO) was diminished in anesthetized dogs undergoing a water diuresis by constriction of the thoracic inferior vena cava (TIVC). In intact animals (group I) acute TIVC constriction decreased CO from 3.5 to 2.2 liters/min (P < 0.005) as urinary osmolality (U(osm)) increased from 103 to 543 mosmols/ kg (P < 0.001) and free water clearance (C(H2o)) decreased from 2.1 to -0.6 ml/min (P < 0.001). This antidiuretic effect was disassociated from changes in renal arterial and venous pressures, glomerular filtration rate, solute excretion, and renal innervation. To examine the role of vasopressin in this antidiuresis, studies (group II) were performed in acutely hypophysectomized, steroid-replaced animals. In these animals TIVC constriction decreased CO to a similar degree from 3.4 to 2.1 liters/min (P < 0.001). However, the effects on U(osm) (87-104 mosmols/kg) and C(H2o) (2.1-1.6 ml/min) were significantly less than in intact dogs. In another group of hypophysectomized animals, (group III) renal arterial and venous pressures were not controlled, and the effect of TIVC constriction on U(osm) was not significant (65-79 mosmols/kg) although C(H2o) decreased from 3.3 to 1.9 ml/min (P < 0.001). In both the group II and III studies, there were linear correlations between the changes in C(H2o) and the urine flow. Studies were also performed in baroreceptor-denervated animals with intact hypothalamo-neurohypophyseal tracts, and acute TIVC constriction altered neither U(osm) nor C(H2o) when renal arterial pressure was controlled. These results therefore indicate that the effect of TIVC constriction on U(osm) is primarily vasopressin mediated while the effect on C(H2o) is mediated both by vasopressin release and diminished distal fluid delivery. A decrease in renal arterial pressure, or some consequence thereof, seems to be an important determinant of the latter effect.

Reduction of compartment compliance increases venous flow pulsatility and lowers apparent vascular compliance: implications for cerebral blood flow hemodynamics.

The global compliance of a fixed-volume, incompressible compartment may play a significant role in determining the inherent vascular compliance. For the intracranial compartment, we propose that the free-displacement of the cerebral spinal fluid (CSF) directly relates to cerebral vascular compliance. To test this hypothesis, an in vivo surrogate intracranial compartment was made by enclosing a rabbit's kidney within a rigid, fluid-filled container. Opening/closing a port atop the box modulated the free flow of box fluid (open-box state). We observed that the pulsatility of the renal venous outflow increased in response to hampering the free flow of fluid in-and-out of the container (closed-box state). To associate the observed pulsatility changes with the compliance changes, a parametric method was proposed for the computation of the apparent compliance (C(app)) of the whole renal vascular system. The calculated C(app) for each experiment's closed-box state was favorably compared to a time-domain compliance assessment method at the mean heart rate. In addition, it was revealed that C(app) in the open-box state was greater than that in the closed-box state only when the calculations were performed at frequencies lower than the heart rate and closer to the ventilation rate. These experimental results support the concept that the vessel compliance of vascular systems enclosed within a rigid compartment is a function of the global compartment compliance.

Renal substrate metabolism and gluconeogenesis during hypoglycemia in humans.

To examine the potential contribution of precursor substrates to renal gluconeogenesis during hypoglycemia, 14 healthy subjects had arterialized hand vein and renal vein (under fluoroscopy) catheterized after an overnight fast. Net renal balance of lactate, glycerol, alanine, and glutamine was determined simultaneously with systemic and renal glucose kinetics using arteriovenous concentration differences and 6-[2H2]glucose tracer dilution. Renal plasma flow was measured by para-aminohippurate clearance and was converted to blood flow using the mathematical value (1-hematocrit). Arterial and renal vein samples were obtained in the postabsorptive state and during a 180-min hyperinsulinemic period during either euglycemia or hypoglycemia. Insulin increased from 49 +/- 14 to 130 +/- 25 pmol/l (hypoglycemia) and to 102 +/- 10 pmol/l (euglycemia). Arterial blood glucose decreased from 4.5 +/-0.2 to 3.0 +/- 0.1 mmol/l during hypoglycemia but did not change during euglycemia (4.3 +/- 0.2 mmol/l). After 150 min, endogenous glucose production reached a plateau value that was higher during hypoglycemia (10.3 +/0.6 micromol x kg(-1) x min(-1)) than during euglycemia (5.73 +/-0.6 micromol x kg(-1) x min(-1), P < 0.001). Hypoglycemia was associated with a rise in renal glucose production (RGP) from 3.0 +/- 0.7 to 5.4 +/- 0.6 micromol x kg(-1) x min(-1) (P < 0.05), although glucose utilization remained the same (2.0 +/- 0.8 vs. 2.1 +/-0.6 micromol x kg(-1) x min(-1)). As a result, net renal glucose output increased from 1.0 +/- 0.3 to 3.3 +/- 0.40 micromol x kg(-1) x min(-1). Elevations in net renal uptake of lactate (2.4 +/- 0.5 to 3.5 +/- 0.7 vs. 2.8 +/- 0.4 micromol x kg(-1) x min(-1)), glycerol (0.6 +/- 0.3 to 1.3 +/- 0.5 vs. 0.4 +/- 0.2 micromol x kg(-1) x min(-1)), and glutamine (0.7 +/- 0.2 to 1.1 +/- 0.3 vs. 0.1 +/- 0.3 micromol x kg(-1) x min(-1)) during hypoglycemia versus euglycemia (P < 0.05) could account for nearly 60% of all glucose carbons released in the renal vein during hypoglycemia. Our data indicate that extraction of circulating gluconeogenic precursors by the kidney is enhanced and responsible for a substantial fraction of the compensatory rise in RGP during sustained hypoglycemia. Increased renal gluconeogenesis from circulating substrates represents an additional physiological mechanism by which the decrease in blood glucose concentration is attenuated in humans.

Gaseous oxygen perfusion of the renal vessels as an adjunct in kidney preservation.

Gaseous oxygen perfusion of the stored kidney provides life-supporting renal function in canine kidneys damaged by 30 min of warm ischaemia followed by cold storage for a total of 24 hr. Other simple methods of renal preservation, including simple flushing and cold storage and oxygenation of the flush solution and the fluid surrounding the kidney during storage, did not result in consistent life-supporting renal function under these experimental conditions. Low pressure venous oxygen perfusion of the kidney produced significantly better renal function than arterial oxygen perfusion as measured by post-transplant creatinine values. This preservation technique uses apparatus readily available in hospitals and once instituted does not require supervision. It may have clinical application in cadaveric renal transplantation, particularly if the donor kidney has been subjected to warm ischaemia.