Renal salt-wasting disease (RSWD) is a rare process characterized by hyponatremia and extracellular fluid volume depletion. This case study details the management of a patient with severe hyponatremia found to be secondary to RSWD. We aim to highlight the challenges in diagnosing, treating, and monitoring RSWD in the intensive care setting, including differentiating RSWD from other hyponatremic pathologies with similar clinical presentations. In this case, we achieved treatment success using multi-modal therapy that included sodium chloride tablets, fludrocortisone, and ibuprofen to restore eunatremia.

Renal salt-wasting disease, Management, Acute and chronic hyponatremia, Multi-model therapy, Treatment.

Renal salt-wasting disease (RSWD) is a complex clinical entity that is often mistaken for the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and cerebral salt-wasting disease (CSWD) due to overlapping symptoms and a similar frequency of diagnosis.[1] RSWD is characterized by excessive renal salt wasting, resulting in hyponatremia and intravascular volume depletion, with altered mental status as a symptom of severe disease.[2] Differential diagnosis and appropriate management are crucial to prevent complications associated with RSWD, such as cerebral edema, seizure, coma, and arrhythmias. In this case study, we present a patient with RSWD, focusing on the diagnostic approach and treatment strategies during his care.

A 76-year-old man was admitted to the hospital for evaluation of increasing confusion following a fall with a head injury. His medical history was notable for alcohol use disorder, chronic hyponatremia, cellulitis, coronary artery disease, and peripheral vascular disease. Initial laboratory investigations revealed severe acute and chronic hyponatremia (sodium of 119 mEq/L), presumed to be secondary to SIADH. The patient was oriented to self and location but had difficulty maintaining a conversation with tangential thoughts & fixations. On admission, we determined the patient to be hypovolemic due to his slow capillary refill, dry mucus membranes, decreased skin turgor, and low urine output.

We confirmed his hypotonic hyponatremic state by basic metabolic panel (BMP) and serum osmolality measurements. Fluid restriction did not increase his serum sodium concentration, nor did he respond to fluid challenges. The differential for these findings included central diseases and peripheral organ-mediated disease. Central diseases considered were SIADH, pituitary injury or failure, hypothyroidism, primary adrenal insufficiency, primary polydipsia, and cerebral salt wasting. Peripheral diseases considered included heart failure, liver failure, Addison’s disease, medication-mediated, and renal salt wasting.

Head trauma was addressed by neurosurgical consultation and appropriate management, with no acute pathology found to explain his hyponatremia. Brain magnetic resonance imaging (MRI) showed an intact pituitary gland with an incidental nonsignificant arteriovenous malformation (AVM). Next, we reviewed his medications, finding no medications that are known to contribute to SIADH. His lab results and clinical findings showed no signs of significant liver disease or heart failure, with an intact hypothalamic–pituitary–adrenal axis.

Our initial management of the severe hyponatremia included free water restriction with intravenous hypertonic 3% saline and oral sodium and potassium repletion. We closely monitored the patient in the Intensive Care Unit (ICU), where he was assessed for neurologic changes, blood pressure, fluid status, and serum and urine electrolyte levels.

Diagnostic tests included measurement of urine sodium concentration and fractional excretion of sodium (FENa). Despite concurrent administration of hypertonic saline, he was salt-wasting as his measured urine sodium excretion exceeded the sodium load given.[2-4] Another method of differentiating RSWD vs. SIADH (with debatable specificity) is by comparing the BUN/Cr ratio. One review showed a trend of blood urea nitrogen (BUN)/Cr being 14-20 in RSW and 15.7-23.3 in SIADH.[5] Our patient had a BUN/Cr ratio of 9.09, which did not narrow the diagnosis.

When our initial management strategy, which included free water restriction and hypertonic saline resuscitation, failed to improve the serum sodium levels, we increased the doses of hypertonic saline. We successfully increased his serum sodium to 130 mg/dl but failed to achieve sustained eunatremia when the hypertonic saline drip was stopped. Ultimately, we utilized sodium chloride tablets (3 grams given thrice daily), 0.2 mg fludrocortisone, and ibuprofen (200 mg thrice daily) to limit renal sodium waste at the tubular level.

The patient’s serum sodium gradually increased during the hospital stay, and hyponatremia was corrected within eight days. His maintenance fluid therapy with hypertonic 3% saline was adjusted based on his fluid balance and repeat sodium levels. His goal sodium level was 130mmol/L, similar to his baseline sodium status. During this time, we could not consistently maintain eunatremia without hypertonic saline, so we pursued the supplemental treatments above. The patient’s mental status improved to complete orientation as his sodium reached baseline, and he was soon able to be discharged home on an oral regimen.

RSWD is thought to be a disease primarily affecting the proximal tubule, which decreases the effective circulating volume (ECV) due to heavy sodium losses, resulting in inappropriate antidiuretic hormone secretion or natriuretic factor imbalance. SIADH is characterized by a non-osmotic release of ADH from the pituitary gland or non-pituitary sources. Differentiation from SIADH is paramount, as treating one disease may worsen the other. SIADH often has a more insidious onset with less severe disease, as defined by minimal to moderate hyponatremia and less altered mental status. Additionally, fluid restriction can often be sufficient to treat SIADH. In contrast, RSWD and CSWD have more severe hyponatremia, altered mental status, and do not respond to fluid restriction.[6] One key differential finding is consistent salt wasting through urination, whereas SIADH may only exhibit transient salt wasting.[1]

On the initial evaluation of this older gentleman with known hyponatremia, we presumed his fall and hyponatremia were related to excessive alcohol consumption and possible poor oral intake secondary to alcohol use. However, his admission ethanol levels were negative, and the toxic alcohol panel was negative. His hyponatremia was surprisingly not accompanied by low serum osmolarity but extraordinarily high urine osmolarity. This raised our suspicion of elevated antidiuretic hormone (ADH) as the driver of his hyponatremia. However, given our clinical impression of volume depletion, we considered the possibility that his normal serum osmolarity was falsely elevated due to hemoconcentration. We therefore aggressively repleted his intravascular volume using isotonic intravenous (IV) fluids, followed by hypertonic IV fluids. When this proved unsuccessful in raising his serum sodium at the expected rate, we re-evaluated our differential diagnosis. Hypo-osmolar hyponatremia now seemed less likely, given his lack of response to an osmole load. Elevated ADH levels became a more significant concern, but evaluations for common causes – pain, nausea, adrenal insufficiency, hypothyroidism, heart failure, liver failure, kidney failure, medications, and increased intracranial pressure – were all negative. We sought alternate explanations for persistent hyponatremia with elevated urine osmolarity. This led us to consider cerebral salt-wasting versus renal salt-wasting disease.

We administered fludrocortisone at 0.1 mg daily for its salt-absorptive effects in the absence of any adrenal pathology. The mineralocorticoid enhances sodium reabsorption in the distal tubules of the kidney and is a beneficial adjunctive therapy in CSWD/RSWD.[6,7] Ibuprofen was utilized for its side effect profile and preliminary evidence of use in CSWD/RSWD. Ibuprofen and nonsteroidal anti-inflammatory drugs (NSAIDs), in general, promote sodium and water retention via multiple mechanisms, including local renal, neural, and hormonal factors. Local effects include limiting the impact of renin, causing hyporeninemic hypoaldosteronism. Neural/hormonal effects include a decrease in prostaglandin-induced inhibition of both renal chloride reabsorption and the action of ADH.[8]

This case study highlights the challenges in diagnosing and managing renal salt-wasting disease. Prompt recognition and differentiation from other hyponatremic conditions, particularly SIADH, are crucial to implementing appropriate treatment strategies. The use of ibuprofen, an often-avoided medication during renal pathologies, was instrumental in achieving eunatremia. Multidisciplinary collaboration, including critical care, nephrology, and neurosurgery, is essential for comprehensive patient care. Regular monitoring and follow-up play a vital role in preventing complications and ensuring successful outcomes in patients with RSWD.

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Corresponding Author:
Hank Weinstock
Department of Anesthesiology
University of Illinois Peoria, USA

Co-Author:
Andrew Donati
Department of Nephrology
Waterbury Hospital, USA

Hank Weinstock and Andrew Donati conceived the treatment approach equally. Hank Weinstock created the manuscript, while Andrew Donati provided supervision and contributed to the manuscript.

The authors are responsible for all aspects of the work, ensuring that any questions regarding the accuracy or integrity of any part are thoroughly investigated and resolved. All procedures conducted in this study complied with the institution’s ethical standards. This case report was published with the consent of the described patient and the patient’s power of attorney.

The author declares no conflict of interest.

None

https://doi.org/10.63096/medtigo3092211

Hank W, Andrew D. Management of Renal Salt-Wasting Disease in a Patient. medtigo J Emerg Med. 2025;2(1):e3092211. doi:10.63096/medtigo3092211 Crossref