Abstract-Persistent proteinuria is considered a deleterious prognostic factor in most progressive renal diseases. However, the mechanisms by which proteinuria induces renal damage remain undetermined. Since proximal tubular cells possess all the machinery to generate angiotensin II (Ang II), we approached the hypothesis that proteinuria could elicit the renal activation of the renin-angiotensin system in a model of intense proteinuria and interstitial nephritis induced by protein overload. After uninephrectomy (UNX), Wistar-Kyoto rats received daily injections of 1 g BSA or saline for 8 days. The mean peak of proteinuria was observed at the fourth day (538Ϯ89 versus 3Ϯ1 mg/24 h in UNX controls; nϭ12; PϽ0.05) and was increased during the whole study period (at the eighth day: 438Ϯ49 mg/24 h; nϭ12; PϭNS). Morphological examination of the kidneys at the end of the study showed marked tubular lesions (atrophy, vacuolization, dilation, and casts), interstitial infiltration of mononuclear cells, and mesangial expansion. In relation to UNX control rats, renal cortex of BSA-overloaded rats showed an increment in the gene expression of angiotensinogen (2.4-fold) and angiotensin-converting enzyme (ACE) (2.1-fold), as well as a diminution in renin gene expression. No changes were observed in angiotensin type 1 (AT 1 ) receptor mRNA expression in both groups of rats. By in situ reverse transcription-polymerase chain reaction and immunohistochemistry, ACE expression (gene and protein) was mainly localized in proximal and distal tubules and in the glomeruli. By immunohistochemistry, angiotensinogen was localized only in proximal tubules, and AT 1 receptor was localized mainly in proximal and distal tubules. In the tubular brush border, an increase in ACE activity was also seen (5.5Ϯ0.5 versus 3.1Ϯ0.7 U/mg protein ϫ10 Ϫ4 in UNX control; nϭ7; PϽ0.05). Our results show that in the kidney of rats with intense proteinuria, ACE and angiotensinogen were upregulated, while gene expression of renin was inhibited and AT 1 was unmodified. On the whole, these data suggest an increase in Ang II intrarenal generation. Since Ang II can elicit renal cell growth and matrix production through the activation of AT 1 receptor, this peptide may be responsible for the tubulointerstitial lesions occurring in this model. These results suggest a novel mechanism by which proteinuria may participate in the progression of renal diseases. (Hypertension. 1999;33:732-739.)

The estimation of volume status is of critical importance in the early management of acute illness. Inappropriate therapy, given when errors in volume assessment go unrecognized, is associated with increased acute mortality rates. Unfortunately, the gold standard of radioisotopic volume measurement is neither rapid nor inexpensive, thus leaving the clinician to rely on less accurate measures. This chapter reviews the available methods of volume assessment in the acute care environment. In addition to the history, physical exam, and standard radiographic techniques for volume assessment, the newer technologies of acoustic cardiography, bedside ultrasound, and bioimpedance are presented.

Congest Heart Fail. 2010;16(4)(suppl 1):S45–S51. ©2010 Wiley Periodicals, Inc.Early in the management of acute illness, it is critically important that volume status is accurately estimated. If inappropriate therapy is given because of errors in volume assessment, acute mortality rates are increased. Unfortunately, as the gold standard of radioisotopic volume measurement is costly and time‐consuming, in the acute care environment clinicians are forced to rely on less accurate measures. In this manuscript, the authors review the currently available techniques of volume assessment for patients presenting with acute illness. In addition to discussing the accuracy of the history, physical examination, and radiography, acoustic cardiography and bedside ultrasonography are presented.

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