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CRS subtype | General considerations and recommended therapies | Caveats/areas for future investigation |
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Acute cardio-renal (CRS 1) | Reduce congestion with diuretics, balance negative fluid balance with intravascular refilling | Infusion versus bolus; dose; electrolyte concerns |
Renin-angiotensin blockade may need to be reduced or even withheld with worsening renal function |
With preserved or elevated blood pressure, empiric use of vasodilators | Limited data from uncontrolled trials; nitroprusside limited by toxicity |
Nesiritide may improve cardiac output and cause significant diuresis | Conflicting results of clinical trials; ongoing trials to determine safety, efficacy, and dose |
With low pressure, poor cardiac output, inotropes may be required as a bridge to recovery or transplantation | Intropes may provoke ischemia or arrhythmia; increased mortality in some studies; mechanical support (balloon pump, ventricular assist device, etc.) may be required |
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Chronic cardio-renal (CRS 2) | Renin-angiotensin blockade is of primary importance; may need to be reduced or withheld with significantly worsening renal function | Most studies have excluded patients with significant kidney disease; increase in creatinine >30% or potassium >5.0 mmol/L cause for concern |
Aldosterone antagonists may be cautiously considered | Creatinine >2.5 mg/dL (>220 μmol/L) or potassium >5.0 mmol/L were exclusions in clinical trials |
Beta-blockers are important adjuncts in congestive heart failure and/or ischemic heart disease | Some agents (atenolol, nadolol, sotalol) have altered pharmacokinetics; carvedilol may have an advantage over older drugs |
Concomitant anemia may worsen symptoms and outcomes | Unclear role of erythropoiesis-stimulating agents; parenteral iron encouraging in terms of symptoms as well as improved renal function |
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Acute reno-cardiac (CRS 3) | Contrast nephropathy is a common example of CRS 3; prevention is likely the best strategy | |
Numerous strategies tested; isotonic fluids and possibly N-acetylcysteine have the best evidence to date | Preexisting chronic kidney disease, age, diabetes, and volume contraction are amongst risks that predispose to contrast nephropathy |
Low osmolar, nonionic contrast may reduce risk of CRS 3 | |
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Chronic reno-cardiac (CRS 4) | Multifaceted disorder with both traditional and non-traditional risk factors; graded risk based on degree of chronic kidney disease | Lifestyle modification (smoking, weight control, activity, and nutrition) of probable benefit but limited evidence |
Anemia closely related to poor outcomes; current guidelines recommend starting for sustained hemoglobin <10 g/dL (100 g/L) and targeting 10–12 g/dL (100–120 g/L) | Studies showed increased harm from higher targets; concerns have been raised about stroke risk, and risk in patients with cancer |
Management of chronic kidney disease-related mineral and bone disorders; phosphate binders, vitamin D analogs, controlling PTH | As yet, efficacy largely limited to putative surrogate endpoints; ongoing trials with hard cardiovascular endpoints awaited |
Lipid lowering with statins | Efficacy in dialysis-dependent patients is questioned; in lesser degrees of chronic kidney disease risk reduction is clearly established |
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Secondary cardio-renal (CRS 5) | Sepsis is a common example of CRS 5; management needs to focus on protecting/optimizing both cardiac and renal function | Other secondary causes of CRS 5 are a fruitful area for ongoing research |
Volume and pressor support to achieve a mean arterial pressure ≥65 mmHg and central venous pressure of 8 to 12 mmHg and adequate oxygen delivery | Early protocol-driven interventions lower risk of adverse renal outcomes and death due to cardiovascular collapse |
Norepinephrine preferred over dopamine in a randomized controlled trial (most patients had septic shock) | Higher incidence of cardiac arrhythmia and trend to increased need for dialysis with dopamine |
Addition of low-dose vasopressin in select patients | May decrease risk of adverse cardiac and renal outcomes |
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