Nephrosclerosis Workup

Updated: Mar 30, 2015
  • Author: Fernando C Fervenza, MD, PhD; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Workup

Laboratory Studies

Based on Joint National Commission (JNC VII) recommendations, [27] there are 3 objectives when evaluating a hypertensive patient: (1) identifying other cardiovascular risk factors, (2) revealing identifiable causes of high BP, and (3) evaluating for evidence of end organ damage.

Laboratory evaluation includes the following:

In a large series of patients, most had urine protein excretion of lower than 1 g/d; however, in some patients with biopsy-proven hypertensive nephrosclerosis, a 24-hour urinary protein excretion greater than 1 g/d has been described. When secondary changes of focal segmental glomerulosclerosis (FSGS) related to hyperfiltration develop, proteinuria can increase to the nephrotic range.

Innes et al (1993) reviewed 185 cases of patients with renal biopsy specimens that were classified solely as hypertensive nephrosclerosis. [28] In 40% of these patients, urinary protein excretion was greater than 1.5 g/d, with 22% excreting more than 3 g/d and 18% having serum albumin values less than 3 g/dL. Similar findings were reported by Harvey et al (1992). [29] Freedman et al (1994) questioned these findings because many biopsy specimens showed segmental and diffuse glomerulosclerosis. [30] Harvey et al attributed these lesions to the effect of hypertension, but Freedman et al believed that these patients had idiopathic FSGS, not hypertensive nephrosclerosis. [29, 30]

The contrasting conclusions of Harvey et al and Freedman et al highlight the problems of distinguishing hypertensive nephrosclerosis from primary glomerular disease purely on clinical grounds. Nevertheless, in black people who are hypertensive, do not have diabetes, and have mild-to-moderate renal failure and proteinuria less than 2 g/d, renal biopsy specimens are likely to show morphological lesions consistent with the clinical diagnosis of hypertensive nephrosclerosis. On the other hand, the diagnosis of hypertensive nephrosclerosis in a young white patient is unusual, and these findings suggest an alternative diagnosis.

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Imaging Studies

An echocardiogram may be required to assess left ventricular size.

Renal imaging with either an ultrasound or an intravenous pyelogram reveals that kidney size is usually symmetric and may be normal or modestly reduced.

The renal calices and pelves are normal.

Renal asymmetry or irregularities in the contour raise the possibility that hypertension could be secondary to renal artery stenosis or reflux nephropathy.

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Other Tests

ECG typically shows left ventricular hypertrophy; however, this may not be evident on the ECG tracings. The sensitivity of ECG in helping to detect left ventricular hypertrophy may be as low as 22%. However, it is recommended as part of the initial evaluation of hypertensive patients (JNC VII).

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Procedures

A definitive diagnosis of hypertensive nephrosclerosis cannot be made without a renal biopsy, especially in the white patient population. In the absence of a renal biopsy, the diagnosis of hypertensive nephrosclerosis is one of exclusion.

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Histologic Findings

Upon gross pathologic examination, the kidneys are shrunken and scarred. According to Tracy and Ishii (2000), the descriptive pathologic abnormalities of benign nephrosclerosis seen on renal biopsy specimens include glomeruli obsolescence, interstitial fibrosis, arterial intimal fibroplasia, arteriolar hyalinization in arterioles (most notably afferent), and small arteries (arcuate and interlobular artery). (Histologic effects on the arcuate artery are seen in the image below.) [4]

Nephrosclerosis. Fibrointimal proliferation of the Nephrosclerosis. Fibrointimal proliferation of the arcuate artery (periodic acid-Schiff stain at 150X magnification).

Myointimal hypertrophy of the interlobular arteries, hyaline degeneration, and sclerosis of afferent arterioles are the most characteristic findings of hypertensive nephrosclerosis. Interlobular arteries often show reduplication of the internal elastic lamina and medial hypertrophy. The arterial wall shows hyaline changes, appearing as eosinophilia, and distinctively periodic acid-Schiff–positive deposits. The arteriolar lumen is narrowed. The image below demonstrates hyaline arteriosclerosis.

Nephrosclerosis. Hyaline arteriosclerosis with hya Nephrosclerosis. Hyaline arteriosclerosis with hyaline deposits (arrows) (trichrome stain at 250X magnification).

Early in the disease process, the glomeruli are normal. With time, ischemic changes become visible, including wrinkling of the glomerular tuft (seen in the image below) and thickening of the Bowman capsule. Occasionally, mild focal mesangial cell proliferation and matrix expansion occur. Eventually, complete glomerular hyalinosis and obsolescence ensue with the development of secondary tubular atrophy and interstitial fibrosis. In contrast, the presence of enlarged glomeruli and the absence of collapse of the basement membrane suggest that the patient is most likely developing secondary FSGS superimposed on primary hypertensive disease.

Nephrosclerosis. The glomerular tuft is shrunken, Nephrosclerosis. The glomerular tuft is shrunken, with wrinkling of the capillary walls (asterisk), global glomerular sclerosis (arrow), and complete obliteration of the capillary loops and glomerular ischemia (periodic acid-Schiff stain at 250X magnification).

With immunofluorescence, no specific pattern is noted, with the exception of an increased prevalence of immunoglobulin M deposits in the arterioles and mesangium. Fibrinoid necrosis and microinfarcts are features of malignant or accelerated hypertension, not nephrosclerosis. Of note, electromicroscopy examination of renal biopsy specimens may help to distinguish primary FSGS from secondary FSGS. In primary FSGS, foot process effacement is widespread; in secondary FSGS, it is more localized.

As noted by Fogo et al (1997), none of the above lesions is pathognomonic. [31] Consider the diagnosis of hypertensive nephrosclerosis only when the constellation of these changes is present in the absence of other lesions of primary glomerular disease.

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