The Evidence of Occult Hypervolemia; Improvement of Cardiac Functions After Kidney Transplantation

Abstract

The term cardiorenal syndrome (CRS) has been used to define interactions between acute or chronic dysfunction of the heart or kidney. When primary chronic kidney disease contribute to cardiac dysfunction, it is classified as type 4 CRS. Cardiac dilatation, valve regurgitations, and left ventricular dysfunction are observed in end-stage renal failure patients with uremic cardiomyopathy. Because of perioperative risks in these patients, they may not be considered a candidate for kidney transplantation. However, uremic cardiomyopathy can be corrected when volume control is achieved by appropriate dose and duration of ultrafiltration. By presenting two cases with occult hypervolemia in uremic cardiomyopathy whose cardiac functions improved early after kidney transplantation, attention is drawn to the importance of kidney transplantation on cardiac function in such patients primarily and the importance of strict volume control on cardiac function in dialysis patients waiting for kidney transplantation.

• occult hypervolemia
• cardiorenal syndrome
• uremic cardiomyopathy
• ultrafiltration
• kidney transplantation

INTRODUCTION

Acute or chronic dysfunction of the heart or kidney can lead to dysfunction of another. The term cardiorenal syndrome (CRS) has been used to define these interactions.¹ Chronic hypervolemia could cause cardiac dilatation, valve regurgitations, and left ventricular dysfunction called uremic cardiomyopathy in end-stage renal disease (ESRD) patients.² In dialysis patients, significant improvements in cardiac functions can be achieved by ultrafiltration and strict volume control.^3–6 By presenting two cases with occult hypervolemia whose cardiac functions improved early after kidney transplantation, attention is drawn to the importance of kidney transplantation on cardiac functions in such patients primarily and the importance of strict volume control on cardiac functions in dialysis patients waiting for kidney transplantation.

CASE REPORT 1

A 42-year-old female patient underwent kidney transplantation from living donor in May 2011. She was on continuous ambulatory peritoneal dialysis treatment for 3 years. She had history of diabetic nephropathy and bilateral nephrolithiasis. She was followed as heart failure with lower ejection fraction. There was no crackle on pulmonary auscultation. Pretibial edema was not detected. She was normotensive. Cardiothoracic index (CTI) was estimated 53% on telecardiography. Preoperative echocardiography showed left heart chamber dilatation, mitral valve regurgitation and lower left ventricular ejection fraction (Table 1). Inferior vena cava index was >50%. After transplantation, the creatinine level decreased to 0.9 mg/dL from 5 mg/dL with functioning graft. She had lost about 4 kg of weight in postoperative period. One and a half months after transplantation, increased left ventricular ejection fraction and decreased cardiac dilatation and valve regurgitation were observed in the control echocardiogram performed by the same cardiologist (Table 1).

Table 1. Echocardiographic parameters of case 1.

	Weight (kg)	LAD (cm)	LVEDD (cm)	LVESD (cm)	IVS (cm)	PWT (cm)	LVM (gr)	MVR (degree)	LVEF (%)
Pretransplant	61	3.7	6.6	5.3	1	0.9	326	2	28
Posttransplant	57	3.4	6.3	5.2	0.8	1	279	1	35

Note: LAD, left atrium diameter; LVEDD, left ventricular end-diastolic diameter; LVESD, left ventricular end-systolic diameter; IVS, interventricular septum thickness; PWT, posterior wall thickness; LVM, left ventricular mass; MVR, mitral valve regurgitation; LVEF, left ventricular ejection fraction (LVEF was estimated with Simpson’s method).

CASE REPORT 2

A 43-year-old male patient underwent kidney transplantation from living donor in June 2011. He was on hemodialysis treatment for 1 month. He had a history of familial Mediterranean fever. He was followed as heart failure with lower ejection fraction. There was no crackle on pulmonary auscultation. Pretibial edema was not detected. He was normotensive. CTI was estimated 51% on telecardiography. Preoperative echocardiography showed left heart chamber dilatation, mitral valve regurgitation and lower left ventricular ejection fraction (Table 2). Inferior vena cava index was >50%. After transplantation, the creatinine level decreased to 2.1 mg/dL from 5 mg/dL with functioning graft. He had lost about 8 kg of weight in postoperative period. One month after transplantation, increased left ventricular ejection fraction and decreased cardiac dilatation and valve regurgitation were observed in the control echocardiogram performed by the same cardiologist (Table 2).

Table 2. Echocardiographic parameters of case 2.

	Weight (kg)	LAD (cm)	LVEDD (cm)	LVESD (cm)	IVS (cm)	PWT (cm)	LVM (gr)	MVR (degree)	LVEF (%)
Pretransplant	86	4	5.8	4.5	0.9	1	258	2	30
Posttransplant	78	3.2	5.4	4.3	1	0.9	227	1	45

Note: LAD, left atrium diameter; LVEDD, left ventricular end-diastolic diameter; LVESD, left ventricular end-systolic diameter; IVS, interventricular septum thickness; PWT, posterior wall thickness; LVM, left ventricular mass; MVR, mitral valve regurgitation; LVEF, left ventricular ejection fraction (LVEF was estimated with Simpson’s method).

DISCUSSION

The term CRS has been used to define interactions between acute or chronic dysfunction of the heart or kidney. Five types of CRS are defined by Ronco et al.¹ While type 1 CRS is acute kidney injury owing to acute heart failure, type 2 CRS is progressive chronic kidney disease owing to chronic cardiac dysfunction. When acute and primary worsening of kidney function lead to acute cardiac dysfunction, it is called as type 3 CRS. While primary chronic kidney disease contribute to cardiac dysfunction, it is classified as type 4 CRS. Type 5 CRS is both cardiac and renal dysfunction owing to acute or chronic systemic disorders. Although case 2 was thought to be type 5 CRS because of amyloidosis, our patients were evaluated as type 4 CRS, because cardiac functions improved after transplantation.

Cardiovascular mortality and morbidity are significantly higher in ESRD patients.⁷ Prognosis in uremic patients with cardiac dilatation, valve regurgitations, and left ventricular dysfunction observed in uremic cardiomyopathy could be poorer.^8,9

Although uremic cardiomyopathy due to particularly hypervolemia and other factors associated with chronic renal failure such as hypertension, anemia, uremic toxins, arterial stiffness, coronary artery disease had previously thought to be irreversible, it was understood that uremic cardiomyopathy could be corrected when the volume control was achieved by appropriate dose and duration of ultrafiltration.^{3–6, 10–12}

Left ventricular pressure overload often leads to left ventricular hypertrophy. Left ventricular dilatation results from left ventricular volume overload and is associated with systolic dysfunction. Considering the negative impact of systolic dysfunction on survival, interventions to correct the occult or overt volume overload could be useful for left ventricular dysfunction and dilatation and survival of patient. Unfortunately, sometimes clinicians could not exhibit sufficient approach to deal with uremic cardiomyopathy. These patients are usually normotensive or hypotensive; therefore, an attempt to reduce hypervolemia may result with symptomatic hypotension. Focusing to uremic toxins on pathophysiology of uremic cardiomyopathy, approaches for the protection of residual renal function and symptomatic problems in achieving the actual dry weight can lead to ignoring volume control in these patients.

In our previous studies, significant improvements of left ventricular ejection fraction, left ventricular hypertrophy, and valve regurgitations have been obtained by ultrafiltration in hypervolemic dialysis patients.^3,13–15 Considering the impact of cardiac functions on quality of life and survival, the importance of a rational approach on ultrafiltration is obvious in this patient group.

Because of perioperative risks in patients with uremic cardiomyopathy, they may not be considered a candidate for kidney transplantation. However, the studies in the literature showing improvement in left ventricular dilatation, mass, and function after a successful kidney transplant are available.^16–18

The improvements in the echocardiographic parameters were also showed in our cases. Our cases were followed as heart failure with low ejection fraction. They had no pulmonary crackles and pretibial edema. Their blood pressures were normotensive. Therefore, hypervolemia were not suspected, clinically. High CTI and heart chamber dilatation are usually detected in heart failure patients with low ejection fraction. Clinicians consider that heart failure can be responsible for these findings. These findings may be indicative of occult hypervolemia, especially in dialysis patients. The improvements in cardiac functions after kidney transplantation even in patients without clinical hypervolemia have suggested that occult hypervolemia could also be in patients with uremic cardiomyopathy, and ultrafiltration should be considered for cardiac functions in the period of transplant waiting list.

CONCLUSION

Hypervolemia may impair cardiac function in patients with ESRD. Kidney transplantation is the best model of ultrafiltration for correction of hypervolemia. Ultrafiltration should be considered for the improvement of cardiac functions, even if clinical hypervolemia is not observed in dialysis patients with heart failure.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.