We adopted a new strategy to increase renal tubular pressure to treat RVH-related AKI .The result showed a significant clinical effect. Urine volume increased from lower than 50 milliliter per day to 500 milliliter per day in the first 24 hours. This physics and mechanics strategy avoided loop diuretic side effects such as diuretic resistance, activating the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS), which could induce prerenal response and reduce renal blood flow(RBF) [17–18]. This strategy aslo avoided hemofiltration method’s side effects such as injury, infection and expensive cost. However, the effect of 500 milliliter urine output per day did not meet clinical requirement of 800-1000 milliliter or more per day for severe volume overload patient with cardiorenal syndrome. Possible reasons are as follows: i)residual effect of antibiotic: meropenem was stopped at the former day of the trial,but residual side effect on the kidneys may still existed; ii) renal venous hypertension as a major factor of affecting renal perfusion still exists: a volume of 500 milliliter fluid reduction did a little influence on severe volume overload and renal A-V pressure diference; iii) hypoproteinemia, The concentration of albumin was 30.9g/L during the trial. Hypoproteinemia may result in renal interstitial edema which in turn results in a reduction of renal perfusion or other effects. No urinary tract infection, urinary tract injury, bleeding or deterioration of renal function occurred during the whole intervention. This strategy is a successful attempt to treat overload in patients with cardiopulmonary syndrome .
Mechanisms Of Kidney Injury Due To Renal Venous Hypertension
In this case study,injecting saline into bladder to increase renal tubular pressure improved anuria of kidney injury.The result is of great significance for exploring the mechanism of kidney injury due to renal venous hypertension.Owing to congestive renal failure depending more on RVH or CVP than on cardiac output, mean arterial pressure and systematic vascular resistance . There may exist other mechanism or mechanisms of RVH related kidney injury. The possible mechanism,independent of the arterial-venous pressure difference mechanism, have been explored by a variety of studies.Intrarenal distribution of renal blood flow was found by some researchers.༻5-9༽but others did not ༻10-11༽. So early studies showed that mild to moderate elevated
RVH(lower than 15mmHg) did not influence peritubular capillary pressure or intratubular pressure [12, 19]. A further increase resulted in a linear increase in pressure in both the tubules and peritubular capillaries,as well as interstitial pressure.In summmary, as renal venous pressure gradually increases, it in turn affects RBF, GFR and then urine output.Latterly, elevated renal interstitial pressure and proximal tubular pressure in renal venous hypertension were reported by all of the related studies༻12-16༽. Interestingly,they were consistent with each other. Expansion of width of Bowman's were found by the latest RVH studies༻15-16༽. Simultaneously,reduced urineoutput were found as well. Given the outfall of tubules is open to low pressure area of outside kidney,this contradiction is a mystery and it may allure us to explore the mechanism.
Based on these previous findings, we proposed a hypothesis that renal tubule compressed or even collapsed under renal venous hypertension condition may be an important pathophysiological mechanism(figure1). In detail, renal venous hypertension result in tubular capillaries expansion and renal interstitial ede ma and expansion, and in turn result in compressing tubule which increase the pressure of Bowman's. Increased Bowman's pressure further leads to a decrease in GFR and compressed or even collapsed tubules impede urine output. At present, it has not been confirmed that renal tubular obstruction or occlusion occur under the condition of renal venous hypertension. The enrolled patient's tubular pressure was elevated by fluid pressure reverse transmission along the urinary tract and achieved diuretic effect. The finding of this study has filled the gap of evidence indirectly. Prior to the trial, 1.96 milliliter residual urinary was detected by bedside ultrasound so as to rule out lower urinary tract obstruction. Upper urinary tract obstruction was excluded after ultrasound examination showed no hydronephrosis in both renal pelvis. These ultrasound image results supported the hypothesis indirectly by exclusing other cause of acute kidney injury.