Skip to ContentGo to accessibility pageKeyboard shortcuts menu
OpenStax Logo
Pharmacology for Nurses

33.2 Renal-Associated Fluid Volume Excess

Pharmacology for Nurses33.2 Renal-Associated Fluid Volume Excess

Learning Outcomes

By the end of this section, you should be able to:

  • 33.2.1 Describe the pathophysiology of fluid volume excess as it relates to the renal system.
  • 33.2.2 Identify clinical manifestations related to fluid volume excess as it relates to the renal system.
  • 33.2.3 Identify the etiology and diagnostic studies related to fluid volume excess as it relates to the renal system.

Fluid Volume Excess and the Kidneys

Fluid volume excess (FVE) is identified as hypervolemia, or increased blood volume. It is related to excessive intake or inadequate output of body water. In critically ill clients, infusion of crystalloid intravenous fluids can cause hypervolemia manifested by FVE. Additional primary causes of FVE include psychogenic water intoxication, syndrome of inappropriate antidiuretic hormone (SIADH), nephrotic syndrome, and liver cirrhosis.

More commonly, FVE is due to damage to the renal system by some other disease state. The compensatory mechanisms that maintain homeostasis can also be diminished or inactivated by inflammatory processes, infections, vascular compromise, obstruction, nephrotoxic molecules, or genetic defects that affect the kidney. Altered kidney function resulting in FVE is often discussed in terms of prerenal, intrinsic renal (or intrarenal), and postrenal causes.

Prerenal Conditions Associated with Fluid Volume Excess

The most common prerenal causes of FVE are altered renal perfusion due to a significant decrease in the circulating blood volume resulting from hemorrhage, hypovolemia, burns, shock states, myocardial infarction and heart failure, or occlusion or stenosis of the renal artery. The altered oxygen level resulting from decreased perfusion damages the renal tubules, and the resulting FVE is relative to the extent of that damage. Depending on the precipitating cause, the cellular injury may be limited to sloughing of the tubule cells into the lumen of the tubule, or the injury may progress to tubular necrosis. Common causes include acute myocardial infarction (AMI), cerebral vascular accident (CVA), and damage from medications or other chemicals.

Intrinsic/Intrarenal Conditions Associated with Fluid Volume Excess

Intrinsic kidney damage resulting in FVE may be due to acute or chronic changes associated with malignant hypertension, ischemia due to transfusion reactions, rhabdomyolysis, nephrotoxic effects of aminoglycoside antibiotics, heavy metals, recreational drugs, contrast media, infections such as acute glomerulonephritis, interstitial diseases including pyelonephritis, acute allergic interstitial nephritis, pressure from tumor growth, or stone formation in the renal pelvis or the ureters. Ischemic damage to the nephrons is intermittently distributed along the nephron, whereas nephrotoxic damage is limited to the proximal tubule.

Postrenal Conditions Associated with Fluid Volume Excess

Obstruction of the urinary tract causes a backflow of urine into the kidneys. This increases intraluminal pressure in the tubules, causes ischemia, and decreases the GFR, resulting in FVE. The common causes of obstruction include benign prostatic hypertrophy, intra-abdominal tumors, neurogenic bladder, and ureteral obstruction that is often caused by edema formation following diagnostic testing.

Clinical Manifestations of Fluid Volume Excess

The manifestations of fluid volume excess may vary according to the specific cause of the excess. Common manifestations of FVE include (Lewis, 2022; Stickel et al., 2019):

  • Edema in dependent soft tissues
  • Ascites
  • Adventitious breath sounds (crackles or rales)
  • Jugular vein distention
  • Rapid weight gain

Diagnostic Studies

Laboratory tests can indicate how much kidney function has been altered by the underlying cause of the FVE. Fluid volume excess decreases sodium, hematocrit, blood urea nitrogen (BUN), and serum osmolarity values. Common laboratory studies include (American Board of Internal Medicine, 2023; Padilla & Abadie, 2022):

  • Glomerular filtration rate: The GFR provides the most accurate laboratory assessment of renal function. Measurement of the actual filtration rate is possible; however, the procedures are costly and expose the client to either an insulin infusion or a radioisotope injection. The calculated estimate of the GFR is the result of a mathematical calculation based on the client’s serum creatinine level, age, sex, ethnicity and weight. The Modification of Diet in Renal Disease (MDRD) Study equation and the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation are the most common equations used for estimating GFR in clients age 18 and over (National Institute of Diabetes and Digestive and Kidney Diseases, n.d.). The value is expressed as the filtration rate in milliliters per minute per average body surface area. The normal range is greater than or equal to 90 mL/minute/1.73 m2. GFR levels associated with FVE may be initially elevated; however, depending on the cause of the alteration and the resulting tubular damage, the GFR may fall below 60 mL/minute.
  • Sodium: The normal serum sodium level is 136–145 mEq/L. Hyponatremia results from increased fluid intake and may be manifested by FVE, depending on the client’s kidney function. Mildly depressed levels may cause nausea and malaise. Moderately depressed levels can cause progressive neurological alterations including headache and lethargy progressing to seizures, coma, and death. Pulmonary edema unrelated to cardiac events has also been reported.
  • Blood urea nitrogen (BUN): The normal BUN ranges from 8–20 mg/dL. The BUN varies inversely with the fluid volume balance; therefore, fluid volume excess will decrease the BUN.
  • Serum albumin: Decreased serum albumin levels result in the movement of fluid from the vascular space to the interstitial space, which increases edema. The normal range is 3.5–5.5 g/dL.
  • Hematocrit: The hematocrit value decreases with hypervolemia. The normal range for females is 37%–47%; for males, it is 42%–50%.
  • Serum osmolality: Serum osmolarity is determined by the concentration of all particles dissolved in a body fluid and is measured as the number of osmoles per liter. The particles are sodium and the sodium anions, which include chloride, bicarbonate, glucose, and urea. Normal serum osmolality is 275–295 mOsm/kg H2O. Decreased serum osmolarity, or hypo-osmolar serum, can be due to psychogenic polydipsia, SIADH, nephrotic syndrome, or liver cirrhosis (Najem et al., 2022).
  • Urine specific gravity: The normal specific gravity of urine is 1.005–1.030. The specific gravity of urine is near 1.000 in a state of fluid volume excess, which indicates dilute urine.

Additional diagnostic studies may include:

  • Ultrasonography of the abdomen, thorax, and vena cava
  • Renal biopsy
  • Chest x-ray
  • Kidney, ureters, and bladder x-ray
  • CT and MRI studies of the kidneys
  • Pulmonary artery pressure monitoring
  • Central venous pressure monitoring
  • Daily weights

Appendix B: Common Abbreviations and Lab Values provides additional reference values.


This book may not be used in the training of large language models or otherwise be ingested into large language models or generative AI offerings without OpenStax's permission.

Want to cite, share, or modify this book? This book uses the Creative Commons Attribution License and you must attribute OpenStax.

Attribution information
  • If you are redistributing all or part of this book in a print format, then you must include on every physical page the following attribution:
    Access for free at
  • If you are redistributing all or part of this book in a digital format, then you must include on every digital page view the following attribution:
    Access for free at
Citation information

© May 15, 2024 OpenStax. Textbook content produced by OpenStax is licensed under a Creative Commons Attribution License . The OpenStax name, OpenStax logo, OpenStax book covers, OpenStax CNX name, and OpenStax CNX logo are not subject to the Creative Commons license and may not be reproduced without the prior and express written consent of Rice University.