Saudi Journal of Kidney Diseases and Transplantation

: 2006  |  Volume : 17  |  Issue : 3  |  Page : 390--394

Hyponatremic Hypertensive Syndrome in an Obese Man with Renal Ischemia

Khawer Saeed 
 Division of Nephrology, King Abdul Aziz Hospital, Makkah, Saudi Arabia

Correspondence Address:
Khawer Saeed
Consultant Physician & nephrologist, Central West Health, 40 Greenwood Avenue, Grandfalls-Windsor, A2A 1S9, Canada


Renovascular hypertension occasionally manifests as an electrolyte disorder. The combination of hyponatremia and renovascular hypertension is known as hyponatremic­hypertensive syndrome. This syndrome was initially reported in children. Here, we describe a 45 year-old Saudi man who was admitted to the hospital with generalized body weakness and inability to walk. He was confused and was noted to have severe hypertension and very low serum sodium and potassium. The patient was recently started on captopril for blood pressure control, which was discontinued because of deterioration of renal function. Color Doppler renal ultrasound, and magnetic resonance angiography confirmed the diagnosis of renal artery stenosis.

How to cite this article:
Saeed K. Hyponatremic Hypertensive Syndrome in an Obese Man with Renal Ischemia.Saudi J Kidney Dis Transpl 2006;17:390-394

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Saeed K. Hyponatremic Hypertensive Syndrome in an Obese Man with Renal Ischemia. Saudi J Kidney Dis Transpl [serial online] 2006 [cited 2023 Jan 29 ];17:390-394
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Full Text


Renovascular hypertension is the most common type of secondary hypertension with a variety of symptoms caused by activation of renin-angiotensin system by ischemic kidneys. Renovascular hypertension associated with hyponatremia is known as hyponatremic­hypertensive syndrome (HHS). This syndrome was initially described in children. [1] Later, HHS was reported in adults. The first case in adults was described in 1952 when Bauer and Forbes reported a 42 year-old man with severe hypertension. His plasma sodium was between 116 and 129 mmol/L. Postmortem examination revealed severe atheromatous left renal artery stenosis. [2] A study describing HHS has been reported from New Zealand involving 32 patients fulfilling the criteria of HHS. The majority of patients were thin women. Almost all were heavy smokers and the underlying pathology was atherosclerosis. [3] We describe here a case of HHS in an adult Saudi man with renal artery stenosis.

 Case Report

A 45-year-old Saudi man, an ex-smoker, was admitted to the hospital with complaints of generalized body weakness for a week, accompanied by severe headaches, vomiting and inability to walk for a day. He was found to be hypertensive a week prior to admission and was initiated on captopril for blood pressure control.

Physical examination revealed an obese man, who was confused. His blood pressure was 190/110 mmHg, pulse 112 (sitting) and 170/ 100 mmHg, pulse 132 (standing), temperature was 36.6°C, and his respiratory rate was 16. His weight was 112.5 kg, height 172 cm, and BMI 38. The optic fundi showed no papilledema, hemorrhage or exudates. The patient's jugular venous distension was esti­mated to be 7 cm. His lungs were clear to auscultation with normal percussion, and the cardiac examination revealed regular rate and rhythm, and no murmurs, rubs or gallops. The abdomen was non-tender, non-distended, and without organomegaly or bruit. There was no peripheral edema. The neurological examination revealed no focal deficits.

Laboratory investigations revealed: hemo­globin 115 g/L, WBC 9.2x 10 x3/µl, platelet count 219 x 10x 3/µl, serum sodium 85 mmol/L, serum potassium 2.0 mmol/L, urea 40 mmol/L, serum creatinine 3.52 mmol/L, creatine phosphokinase (CPK) 2670 U/L, AST 76 U/L, ALP 245 U/L, calcium 1.75mmol/L, PO4 0.75 mmol/L, and serum albumin 45 g/L. The arterial blood gases revealed pH 7.5, pCO 2 17.5 mmHg, and HCO 3 14 mmol/L. The thyroid function was within normal limits. Urine analysis revealed urine pH 7, while the rest of the examination was unremarkable. The 24-hour urinary volume was 4000 ml and revealed creatinine clearance of 26.5 ml/min, and urinary sodium of 53mmol/L.

The patient's renal ultrasound revealed right kidney length of 7.3 cm, left kidney length of 10.2cm, with mild impairment in cortico­medullary distinction. Color Doppler was performed to rule out renal artery stenosis, which was suggestive of bilateral renal artery stenoses [Figure 1],[Figure 2]. Magnetic resonance angiography (MRA) confirmed the presence of bilateral renal artery stenoses. [Figure 3],[Figure 4].

We switched the captopril to a beta blocker. After 2 weeks, the serum sodium was 131 mmol/L; serum potassium 3.5 mmol/L, serum creatinine 350 mmol/L and CPK 105 U/L. After two months of calcium replacement, the serum calcium improved to 2.1 mmol/L.


In this case, the patient was hypertensive, orthostatic and his serum sodium much lower than that documented in the literature. [2] HHS is not rare but an under recognized disorder. Our patient, contrary to the thin women described in the literature, was an obese man. [4] He was a heavy smoker but quit smoking twenty years ago.

This is an interesting case in which the patient was admitted with a history of vomiting, poly­uria with generalized body weakness and inability to walk. He was hypertensive, ortho­static and confused. These features can be explained by hypertensive encephalopathy which results from breakdown of cerebral autoregulation due to abrupt elevation of blood pressure above the baseline. Fluctuations and variations in cerebral circulation might be the reason for various presenting neurological symptoms. This might explain the extra­ordinary symptoms of altered mental status in our patient without any other neurological abnormalities. Similar concepts and features have been documented in animal and human studies.[5],[6],[7],[8],[9]

The patient had low sodium and potassium was and elevated CPK probably secondary to hypokalemia. In addition, the patient's renal function deteriorated due to captopril. There­fore, we suspected HHS caused by renal artery stenosis. The high intake of water resulted in polyuria in addition to hemodilution of body fluids causing hyponatremia in the presence of renal artery stenosis and impair­ment of renal function.[8]

Atkinson et al. explained the pathology of HHS as being a result of "critical" renal ischemia, and an activated renin-angiotensin system that cause increased blood pressure and induce pressure natriuresis leading to volume depletion and further increase of renin release from ischemic kidneys. [10] Potassium deficiencies may further stimulate renin release and intensify the vicious cycle.[11],[12],[13],[14] Atkinson 's description of the pathophysiology of the HHS was supported by Barraclough who documented this syndrome in a patient with unilateral ischemia. [15]

A characteristic feature of HHS is an association with heavy smoking. Our patient smoked heavily for five years. Nicholson et al found an association between cigarette smoking and renal artery stenosis, whether the pathology was atherosclerotic or fibro-muscular disease. Furthermore, nicotine can be a potent stimulus to antidiuretic hormone (ADH) release causing hyponatremia.[16],[17]

Another feature reported in HHS with renal ischemia is proteinuria, which is sometimes nephrotic range. [18] Our patient did not have nephrotic range proteinuria.

Hyponatremia and hypokalemia disappeared upon normalization of hypertension, while hypercalcemia lasted for several months, probably reflecting the need to restore the enzyme repertoire for tubular re-absorption of Ca. This association of severe arterial hypertension/ renal artery stenosis with mixed urinary findings (glomerular and tubular) and diffuse (proxi­mal and distal convoluted tubule) renal defects was documented by Trivelli et al.[19]

Response to surgery, angioplasty, and drug therapy cannot be ascertained from studies or literature at this time. There is a need for a prospective randomized clinical trial comparing surgical therapies to interventional and aggressive medical management in patients with diffuse atherosclerosis. However, patients with bilateral renal artery stenoses and stenosis in a solitary functioning kidney are candi­dates for revascularization, regardless of renal insufficiency.

Possible medical management include smoking cessation, low goal blood pressure, lowering of cholesterol as per guidelines, aspirin, folate administration, exercise and prudent diet, to deliver optimal care. If the patient has been stable on medical management, there is no need of invasive procedures. If renal function deteriorates or blood pressure cannot be controlled by medical management, then invasive procedures should be considered.

In summary, the diagnosis of renal artery stenosis should be considered in any hyper­tensive presenting with impaired consciousness and weakness associated with hyponatremia and serum and urinary findings suggestive of mixed glomerular and tubular defects.


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