Goodpasture\'s syndrome (GPS) is a rare small vessel vasculitis characterized by circulating antibodies directed against the glomerular and alveolar basement membrane leading to renal and pulmonary manifestations. Here, we discuss a unique case of a 30-year-old Caucasian male smoker initially presenting with hemoptysis and anemia who was found to have biopsy-proven GPS with elevated anti-glomerular basement membrane (anti-GBM) antibodies. Unfortunately, the patient failed four months of standard treatment for GPS leading to end-stage renal disease (ESRD), while uniquely developing cardiorenal syndrome (CRS) with non-ischemic cardiomyopathy resulting in systolic and diastolic heart failure (HF). Despite aggressive medical management and hemodialysis, the patient\'s cardiac function continued to decline and the decision was made to insert an automatic implantable cardioverter defibrillator (AICD). To our knowledge, this is the first reported case of an anti-GBM-positive GPS patient who developed dilated cardiomyopathy. The importance of this report is to illustrate the rarity of developing CRS with non-ischemic cardiomyopathy and congestive heart failure from GPS and highlight the difficulty of determining management changes beyond guideline-directed medical therapy (GDMT) in GPS to slow the progression of worsening cardiac function.

Congestive nephropathy is an underappreciated manifestation of cardiorenal syndrome and is characterized by a potentially reversible kidney dysfunction caused by a reduced renal venous outflow secondary to right-sided heart failure or intra-abdominal hypertension. To date, the histological diagnostic criteria for congestive nephropathy have not been defined. We herein report a case of acute renal dysfunction following cardiac allograft failure and present a review of the relevant literature to elucidate the current understanding of the disease. Our case demonstrated that congestion-driven nephropathy may be histopathologically characterized by markedly dilated veins and peritubular capillaries, focally accentuated low-grade acute tubular damage, small areas of interstitial fibrosis, and tubular atrophy on a background of normal glomeruli and predominantly normal tubular cell differentiation.

Inadequate peripheral perfusion due to cardiac diseases can worsen renal function in patients with chronic kidney disease (CKD). Due to the nature of the simultaneous cardiac and renal disease, it is often difficult to determine which is the primary cause, and hence many surgeons hesitate to operate on patients with end-stage kidney disease. However, when the primary cause is cardiac related, renal function can improve after successful cardiac surgery. Here, we describe a 55-year-old female patient with CKD Stage 5 who was on maintenance hemodialysis with severe aortic stenosis (AS) and underwent surgical aortic valve replacement and recovered from dialysis-dependent kidney disease. Drastic improvement in renal function after cardiac surgery can occur even in patients with CKD due to improved renal perfusion, especially in cases of AS. Therefore, diagnosing the primary cause of renal dysfunction is essential.

Streptococcal infection is a common cause of acute glomerulonephritis. Cardiac damage associated with streptococcal infection commonly occurs in acute rheumatic fever. However, cases of acute non-rheumatic streptococcal myocarditis have been reported in recent years. We report a novel case of concurrent acute glomerulonephritis and non-rheumatic myocarditis following streptococcal infection. A good prognosis was achieved with antibiotic and immunosuppressive therapy, indicating that Streptococcus causes cardiorenal syndrome type 5 via an immune-mediated response. A better understanding of post-streptococcal cardiorenal syndrome is warranted to enable the early diagnosis and treatment of affected patients.

Supercentenarians, people who have reached 110 years of age, represent an ultimate model of human longevity. We have conducted research from both biomedical and psychosocial perspectives to clarify the factors that contribute to healthy longevity. The current study described the clinical course of the oldest lived man in the world.
Kimura Jiroemon, who is the verified oldest man in recorded history, lived for more than 116 years. We conducted a longitudinal investigation including physical and psychological assessments, blood data, and electrocardiogram (ECG) from the age of 111 and obtained medical data such as computed tomography (CT) images during the course of hospitalizations in the last year of his life.
At the age of 111, Jiroemon was almost independent regarding activities of daily living. Additionally, his Philadelphia Geriatric Center Morale Scale score was 15/17, indicating high psychological well-being. His biological data included first-degree atrioventricular (AV) block on ECG; mild decreases of hemoglobin (11.6 g/dL), hematocrit (36.2%), and albumin levels (3.5 g/dL); and elevated serum cystatin C levels (1.32 mg/L), indicating potential dysfunction of the renal and electrical conduction systems. He then lived without fatal illness until the age of 115 years. At this age, he lost consciousness, and his ECG revealed complete AV block. At the first hospitalization for intensive examination, his doctor recommended implanting a cardiac pacemaker, but he and his family declined. On December 12, 2012, his condition rapidly worsened, and he was hospitalized twice for heart failure because of AV block. On May 11, 2013, he lost consciousness after breakfast, and he was hospitalized for the fourth time. He was diagnosed with pneumonia and heart failure based on his chest CT findings and elevated brain natriuretic peptide levels (160 pg/mL), and died on June 12, 2013 at the age of 116.
Despite having no cardiovascular risk factors throughout his life, Jiroemon developed heart failure from potential heart and kidney dysfunction, suggesting that aging of the cardiorenal system was the ultimate pathology of the oldest man in the world. His clinical course represents a model of both suppression of morbidity and extreme longevity. Comprehensive health and longevity research studies from physical and psychological aspects are required.

We present a case of severe diuretic resistance and edema from acute cardiorenal syndrome complicating heart failure with preserved ejection fraction (HFpEF) and mild alcoholic liver disease. High doses of intravenous (iv) furosemide plus iv doses of chlorothiazide failed to increase the daily urine output (UV) above 1,500 mL or the fractional excretion of sodium (FENa) above 2%. The addition of a relatively low dose of hydralazine (10 mg thrice daily PO) during 5 days of constant iv infusion of furosemide plus iv bolus chlorothiazide doubled the UV and FENa while reducing the serum creatinine concentration from 3.3 to 2.0 mg/dL. Hydralazine may have restored a response to the diuretics by increasing the renal blood flow and thereby the renal diuretic delivery, or by reducing the filtration fraction or reducing the renal congestion and thereby reducing the proximal reabsorption during blockade of distal reabsorption with diuretics. Further mechanistic studies of low-dose hydralazine for diuretic resistance are warranted.

Monitoring venous congestion by ultrasound assessment of hepatic venogram allowed individualized fluid management in severe cardiorenal syndrome type 5 due to light chain myeloma, preserving residual renal function and avoiding heart failure.

Cardiorenal syndrome (CRS) is a group of pathophysiological disorders affecting heart and kidneys.
We present 44-year-old kidney transplant recipient with acute-on-chronic graft failure in the course of CRS due to acutely decompensated heart failure associated with severe aortic regurgitation successfully treated with aortic valve replacement. Because of graft failure progression and difficult to eradicate infections he was treated with dialysis and radical minimization of immunosuppression. After 74 days of renal replacement therapy the patient regained graft function after successful aortic valve replacement. The dialysis could be stopped and immunosuppressive therapy was reintroduced. Heart and renal function are stable and patient is doing well without dialysis for 3 years.
The return of kidney graft function can occur even after a long period of dialysis therapy due to improved cardiovascular function. Therefore, distinguishing an acute-on-chronic CRS subtype is mandatory to enable specific patient approach.

Severe aortic stenosis (AS) may lead to acute decompensated heart failure resistant to medical treatment. Here, we report a successful emergent transcatheter aortic valve replacement (TAVR) in a patient presenting with decompensated severe AS accompanied by cardiorenal syndrome.
A 82-year-old man presented at our emergency department with aggravated dyspnea. His chest X-ray showed bilateral pulmonary edema, and laboratory examination revealed acute kidney injury. Transthoracic echocardiography (TTE) revealed low-flow, low-gradient AS with decreased left ventricular systolic function. With a diagnosis of acute decompensated heart failure combined with cardiorenal syndrome, we opted to perform emergent TAVR. Ultimately, we successfully performed emergent TAVR using only TTE and 3-D transesophageal echocardiography (TEE) measurements.
This report presents a case of decompensated severe AS accompanied by cardiorenal syndrome that was treated successfully with emergent TAVR. Thus, emergent TAVR using only echocardiography measurements is a feasible and safe option for treating decompensated heart failure accompanied by cardiorenal syndrome the clinical setting.