Heart Fail Rev. 2011 Nov;16(6):615-20. doi: 10.1007/s10741-010-9197-z.

Hypertension, left ventricular hypertrophy and chronic kidney

disease.
Taddei S1, Nami R, Bruno RM, Quatrini I, Nuti R.
Author information
Abstract
Left ventricular hypertrophy (LVH) is a cardiovascular complication highly prevalent in patients with
chronic kidney disease (CKD) and end-stage renal disease. LVH in CKD patients has generally a
negative prognostic value, because it represents an independent risk factor for the development of
arrhythmias, sudden death, heart failure and ischemic heart disease. LVH in CKD patients is secondary to
both pressure and volume overload. Pressure overload is secondary to preexisting hypertension, but also
to a loss of elasticity of the vessels and to vascular calcifications, leading to augmented pulse pressure.
Anemia and the retention of sodium and water secondary to decreased renal function are responsible for
volume overload, determining a hyperdynamic state. In particular, the correction of anemia with
erythropoietin in CKD patients is advantageous, since it determines LVH reduction. Other risk factors for
LVH in CKD patients are documented: some are specific to CKD, as mineral metabolism disorders
(hypocalcemia, hyperphosphatemia, low serum vitamin D levels and secondary hyperparathyroidism),
others are non-traditional, such as increased asymmetric dimethylarginine, oxidative stress,
hyperhomocysteinemia and endothelial dysfunction that, in turn, accelerates the process of
atherogenesis, triggers the inflammation and pro-thrombotic state of the glomerular and the vascular
endothelium and aggravates the process of both CKD and LVH.

Anemia and left ventricular hypertrophy in chronic kidney

disease
Author
Jeffrey S Berns, MD
Section Editors
Steve J Schwab, MD
Gary C Curhan, MD, ScD
Deputy Editor
Alice M Sheridan, MD

INTRODUCTION
Cardiac disease, including coronary artery disease, left ventricular hypertrophy (LVH) and heart failure
(HF), is common in patients with chronic kidney disease (CKD). LVH appears to be increasingly prevalent
as the glomerular filtration rate (GFR) declines and with increased dialysis vintage:
LVH has been found in as many as 47 percent of patients with CKD not yet on dialysis, with a
higher prevalence and more severe LVH in those with increasingly lower degrees of kidney function
[1-4].

Concentric LVH has been documented by echocardiography in 42 percent of patients at the start of
dialysis [5] and in as many as 75 percent of patients who have been on hemodialysis for 10 years
[6].
LVH is an important predictor of mortality in patients with CKD [5,7-10]. As examples:
In a prospective study of 1249 older subjects with relatively mild CKD (mean GFR of
50 mL/min per 1.73 m2), the presence of LVH was associated with an excess of 25
cardiovascular deaths/1000 patient-years [10]. This was a greater absolute risk than that associated
with diabetes mellitus, smoking, and systolic hypertension.

Send to:
Adv Chronic Kidney Dis. 2008 Jul;15(3):284-96. doi: 10.1053/j.ackd.2008.04.008.

Pulmonary complications after acute kidney injury.

Faubel S1.

Author information
Abstract
The development of respiratory failure in patients with AKI is a particularly devastating consequence that
greatly increases patient mortality. When respiratory failure and AKI occur together, the mortality is
greater than 80%. A clear understanding of the mechanisms leading to respiratory failure is of great
clinical relevance to patients with AKI in order to prevent and treat this life-threatening complication.
Pulmonary edema leading to respiratory failure has been a recognized complication of kidney failure
since 1901. Remarkably, the pathogenesis of this complication remains elusive, despite over 100 years of
clinical and experimental debate in the literature. A review of this literature suggests that there are 4
causes of pulmonary edema leading to respiratory failure in patients with AKI: (1) volume overload
(cardiogenic edema), (2) left ventricular dysfunction (cardiogenic edema), (3) increased lung capillary
permeability (noncardiogenic edema), and (4) acute lung injury (noncardiogenic edema with
inflammation). In this review, these mechanisms are presented in historical context including the original
descriptions of pathology and pathophysiology, recent epidemiologic data, and experimental studies in
animals. Although volume overload is a well-accepted mechanism of pulmonary edema in patients with
AKI, the purpose of this review was to highlight the evidence showing that noncardiogenic edema and
acute lung injury also occur. By recognizing that the pulmonary complications of AKI are not simply from
volume overload, specific treatment strategies may be discovered and used to improve outcomes in
patients with the ominous and life threatening combination of AKI and respiratory failure.
PMID:

18565479

[PubMed - indexed for MEDLINE]

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