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Cardiorenal syndrome is a bidirectional entity involving hemodynamic, neurohormonal and inflammatory factors.
A 69-year-old patient with a history of diabetes mellitus, arterial hypertension, congestive heart failure (CHF), corpulmonary, severe pulmonary hypertension, grade IV chronic kidney disease, cardiorenal syndrome type II and sinus node disease with a pacemaker The clinical picture after 72 h of evolution was characterized by the progression of dyspnea functional class II to IV, orthopnea, asthenia, adynamia, hyperoxia, progressive symmetrical edema in the lower limbs. On admission with BP 100/60 mmhg, hypoventilation in pulmonary bases, systolic murmur grade III/IV in tricuspid focus, jugular ingurgitation 2/3 without collapse with positive hepatojugular reflux, lower extremities with bilateral edema, symmetrical godet (++). Chest X-ray with data of pulmonary edema, pleural effusion in the right hemithorax, and data of cardiomegaly grade I–II at the expense of the right cavities. Laboratory tests: hemoglobin 5.2 g/dL, hematocrit 16.5%, MCV 89 fL and HbCM 28.1 pg; hyperazotemia; hypertransaminasemia; GPT/LDH ratio 0.3; hyperbilirubinemia. Ultrasound was performed with the VEXUS protocol [image 1].
Transthoracic echocardiogram: reported significant dilatation of the right chambers and left atrium; left ventricular remodeling; LVEF 69%; moderate tricuspid insufficiency; severe pulmonary hypertension PSAP 100 mmhg.
Evolved with hypotension 80/50 mmhg, oliguria refractory to diuretic (120 mg Furosemide and 3% hypertonic solution), painful hepatomegaly at 5 cm below the costal ridge, lower limbs with increased godet edema (+++). Diagnoses of cardiogenic shock, acute liver injury due to ischemic hepatitis secondary to decompensated CHF, exacerbated chronic renal disease, cardio renal syndrome type II and normocytic normochromic anemia.
In the clinical context, he was admitted to the ICU, starting vasoactive and inotropic agents and Continuous Kidney Support Therapy (CKRT) in the venovenous hemodiafiltration modality (VVHDF), with UF 5000 ml in the first 24 h, and continuing with CKRT for 72 h, achieving an accumulated negative balance of 11 liters. He progressed the first week with a gradual decrease in vasoactive and inotropic agents, a decrease in venous congestion, and maintaining high values of azoados, so he continued with intermittent Renal Support Therapy. Due to clinical improvement, hospital discharge was granted for outpatient follow-up with Dapagliflozin, Spironolactone, Sacubitril/Valsartan and two months later there was evidence of a progressive decrease in azoados [image 2], for which reason dialytic treatment was suspended and he continues to be followed up by outpatient.
Cardiorenal syndrome is associated with increased mortality. Venous congestion has a deleterious impact on renal and hepatic function whose characteristic is secondary to ischemia, where the GPT/LDH ratio is of great help in the diagnosis. Where one of the fundamental pillars is the use of diuretics alone at high doses or a combination of diuretics, in case of diuretic resistance an alternative is Extracorporeal Support Therapy in SCUF modality when renal function is preserved and in those with renal deterioration and hemodynamic instability an alternative is CKRT in VVHDF or VVHF modality.