Venous congestion has emerged as an important cause of renal dysfunction in patients with cardiorenal syndrome. However, only limited progress has been made in differentiating this haemodynamic phenotype of renal dysfunction, because of a significant overlap with pre-existing renal impairment due to long-term hypertension, diabetes, and renovascular disease. We propose congestive nephropathy (CN) as this neglected clinical entity. CN is a potentially reversible subtype of renal dysfunction associated with declining renal venous outflow and progressively increasing renal interstitial pressure. Venous congestion may lead to a vicious cycle of hormonal activation, increased intra-abdominal pressure, excessive renal tubular sodium reabsorption, and volume overload, leading to further right ventricular (RV) stress. Ultimately, renal replacement therapy may be required to relieve diuretic-resistant congestion. Effective decongestion could preserve or improve renal function. Congestive acute kidney injury may not be associated with cellular damage, and complete renal function restoration may be a confirmatory diagnostic criterion. In contrast, a persistently low renal perfusion pressure might induce renal dysfunction and histopathological lesions with time. Thus, urinary markers may differ. CN is mostly seen in biventricular heart failure but may also occur secondary to pulmonary arterial hypertension and elevated intra-abdominal pressure. An increase in central venous pressure to >6 mmHg is associated with a steep decrease in glomerular filtration rate. However, the central venous pressure range that can provide an optimal balance of RV and renal function remains to be determined. We propose criteria to identify cardiorenal syndrome subgroups likely to benefit from decongestive or pulmonary hypertension-specific therapies and suggest areas for future research.

Increased central venous pressure in congestive heart failure causes renal dysfunction; however, the underlying mechanisms are unclear. We created a rat renal congestion model and investigated the effect of renal congestion on hemodynamics and molecular mechanisms. The inferior vena cava (IVC) between the renal veins was ligated by suture in male Sprague-Dawley rats to increase upstream IVC pressure and induce congestion in the left kidney only. Left kidney congestion reduced renal blood flow, glomerular filtration rate, and increased renal interstitial hydrostatic pressure. Tubulointerstitial and glomerular injury and medullary thick ascending limb hypoxia were observed only in the congestive kidneys. Molecules related to extracellular matrix expansion, tubular injury, and focal adhesion were upregulated in microarray analysis. Renal decapsulation ameliorated the tubulointerstitial injury. Electron microscopy captured pericyte detachment in the congestive kidneys. Transgelin and platelet-derived growth factor receptors, as indicators of pericyte-myofibroblast transition, were upregulated in the pericytes and the adjacent interstitium. With the compression of the peritubular capillaries and tubules, hypoxia and physical stress induce pericyte detachment, which could result in extracellular matrix expansion and tubular injury in renal congestion.

To compare renal dysfunction after right nephrectomy and ligation of the right renal vein with preservation of kidney.

Animals' weight, pH, density, protein in urine and histological samples of the kidneys were evaluated. Fifteen female rats (Wistar) were divided into three groups. In the control group, right renal vein dissections were performed. In the second group, the right nephrectomy was performed. In the third group, the right renal vein was ligated and the kidney was preserved. Urine samples were taken before, three and seven days after the procedure. On the seventh postoperative day the kidneys were removed to histopathological study. Analysis by Student's t test was performed.

weight loss, alterations of urine pH (p<0.05), in specific gravity, proteinuria (p<0.05) were found in groups 2 and 3; hemorrhagic infarction and edema were found after ligation of the right renal vein; changes in the left kidney were also observed on the seventh day.

In cases of trauma to the left renal vein (LRV), its ligation near the inferior vena cava (IVC) is considered, but the consequences are not always good. We investigated the role of collateral venous drainage after ligation of the LRV by studying the renal function and histology after ligation of the LRV near the IVC alone or with ligation of the gonadal or adrenal collaterals, in right-nephrectomized (RN) rats.

Ligation of the LRV near the IVC alone (group 1) or with ligation of the adrenal (group 2) or gonadal (group 3) collaterals was studied in RN Wistar rats (n=18 per group). The renal histopathology (ischemic cortical necrosis) and functional status (urea, creatinine, sodium, and potassium) were compared.

In RN rats, the results were better when ligating the LRV near the IVC alone or with the adrenal collaterals [mortality 4/18 (22.2%) and 3/18 (16.7%), respectively] than when ligating the LRV near the IVC plus the gonadal collaterals [mortality 15/18 (83.3%)] (p<0.0001). All early deaths occurred within three days and resulted from serious histopathological (ischemic cortical necrosis) and functional (increased urea, creatinine, and potassium; decreased sodium) renal damage.

In right-nephrectomized rats, the LRV near the IVC and the adrenal collateral can be ligated, while the gonadal collateral should be preserved.

Experiments involving injection of radio-iodinated albumin into the left renal arteries or left ureters of dogs indicate that the renal lymphatics are capable of a major contribution in returning to the circulation albumin (or other large molecules) escaping from renal capillaries. I131-albumin was injected into the jugular vein of controls or into the left renal artery or in retrograde manner into the left ureter of female dogs. Experimental groups included those with no obstruction, occlusion of left renal veins or left renal lymphatics, or both. Collections were made from the right femoral artery, both renal veins, thoracic duct and both ureters at frequent intervals for 2 to 4 hours. Data analysis included I131 concentration, specific activity, rate of recovery and selected ratios. After renal arterial injection, the percentage of I131 recovered in thoracic duct lymph of dogs without renal venous obstruction was 5 to 10 times that recovered in those that received injections into the jugular vein. In dogs with renal venous obstruction, recovery from the thoracic duct was 10 to 1,000 times that in control dogs. Most of the differences occurred during the first hour, after which time as recirculation and redistribution occurred the rates of appearance in thoracic duct lymph in each group were similar. The differences in the ratios of concentration in thoracic duct lymph to concentration in femoral arterial blood were also much greater when the renal vein was obstructed than in dogs with no obstruction. The greater return of albumin through the thoracic duct in those with impeded renal venous outflow was probably related to both sequestered concentration and increased intrarenal pressure.(ABSTRACT TRUNCATED AT 250 WORDS)