A 65 year old woman with CKD (urate nephropathy) with severe chronic asymptomatic hyponatremia (S-Na 121 mmol/L), elevation of creatinin kinase (7 ukat/L), polyuria (3600ml/day), polydipsia. No episodes of seizures, no clinical signs of dehydration, no medications affecting diuresis or natriuresis.
Serum Na 121, K 4, Cl 82, P 1.31, Ca 2.5, urea 9.2 mmol/L, OSM 254 mmol/kg, creatinine 97 umol/L, CK 7 ukat/L.
Urine Na 36, K 9, Cl 26 , P 3.7, Ca 0.21, urea 59, creatinine 1.28 mmol/L, OSM 147 mmol/kg.
Fractional excretion of Na 2.25%, OSM 4.4%, water 7.6%, urea 48.6%.
pH 7.41, pCO2 5.9 kPa, HCO3 28 mmol/L. Creatinine clearance 0.56 ml/s.
After 4 hours of fluid restriction diuresis was 400ml, increased urine osmolality from 147 to 265 mmol/L, increased urine sodium from 36 to 57 mmol/l, slightly decreased serum osmolality from 254 to 252 mmol/kg, serum sodium remained unchanged.
What is the diagnosis?
Is it water diuresis? Serum osmolality is higher than urinary, but fractional excretion of osmolal substances is high.
Could be primary polydipsia - urine osmolality increased after water restriction, so probably it is not diabetes insipidus, ADH should be present, at least partially.
Why did serum sodium not increase after fluid restriction? Could it be the combination of primary polydipsia and decreased tubular reabsorption of sodium (urate nephropathy)? Why is CK elevated without episodes of seizures?
Thank you for your opinions.
Diabetes insipidus shows hypernatremia, so diabetes insipidus could be excluded in this case.
In this case the renal natrium lost is inadequate high, compared with the low serum natrium levels, so we see a renal natrium lost.
Reasons for this could be: SIADH, hypocortisolism, hypothyreosis.
This 65 year old woman suffered from chronic hyponatremia, polyuria and obligatory NaCl renal lost secondary chronic pyelonephritis linked to urate lithiasis.
With a urine Na of 36 mmol/l and a polyuria of 3,6 liters by day, the urinary loss was 1296 mmol by day, i.e 8,4 NaCl daily obligatory loss.
In absence of hypercalcemia, of medications affecting diuresis and natriuresis, we may suspect an inadequate salt restriction for hypertension (?), cardiac failure (?) or her chronic kidney disease.
Very frequently patients or physicians consider that CKD should be systematically associated with salt restriction regimen, whereas patients with salt wasting tubulopathy suffer of hypovolemia associated with hyponatremia.
SALT RESTRICTION REGIME WORSENS SALT WASTING TUBULOPATHY inherited or acquired (+++).
In clinical practice, a water restriction for two to three days associated with a 12 g Nacl daily intake may correct cellular hyperhydration.
The moderate rhabdomyolisis, in absence of statin, could be secondary to the chronic hyponatremia, even in absence of seizures;
Thank you, dr. Bergner. Diabetes insipidus was mentioned just because of polyuria with water diuresis (as a potential component of combined etiology - decreased sensitivity to ADH due to the interstitial nephritis).
SIADH is not associated with polyuria. TSH and fT4 were in the reference ranges.
We did not measure the level of cortisol, but except of hyponatremia were not present any of the typical signs of hypocortisolism: hyperkalemia, decreased kaliuresis, metabolic acidosis. There were no clinical symptoms as weakness, hypotension etc.
Thank you very much dr. Brivet. We agree that the cause of sodium loss is the salt-losing nephropathy secondary to chronic interstitial nephritis. It is supported by higher actual fractional sodium excretion compared to adequate fractional sodium excretion, 2,25% vs 1,9%. But the question is why the urine osmolality is so low. Free water clearance was 1560ml/day (diuresis 3600ml/day). In my opinion there are two possibilities: 1) decreased concentration ability due to the chronic interstitial nephritis (destruction of renal architecture and/or decreased sensitivity to ADH); 2) high water intake (primary polydipsia). Both together with decreased sodium reabsorption, i.e. salt-losing nephropathy in this case. We recommended the same as you suggested - a water restriction associated with high salt intake.
It is perfectly reasonable for the tubular defect associated with chronic tubulo-interstitial nephritis to result in an inability to concentrate the urine.
Thank you, dr. Smith. Actually, I'd like to know, theoretically, if it is possible to exclude primary polydipsia as a cause of low urinary osmolality in this case using the data mentioned above.
primary polydipsia can be excluded , in view of the salt wasting,
in case of psychiatric poltydipsia, natremia is normal and urinary Na reflects the salt intake.
thus salt wasting tubulopathy remains my primary diagnosis
I agree salt loss makes primary polydipsia unlikely. A water deprivation test would confirm but is unpleasant for the patient and only really of academic interest. Has the renal diagnosis been confirmed? Salt replacement is normal treatment for salt wasting tubulopathies. Often as sodium bicarbonate as bicarbonate is often lost as well. Salt restriction is only needed in glomerulopathies and advanced renal disease where sodium retention and hypertension are the norm
I have no doubt about the presence of salt wasting tubulopathy, but it explains only a part of polyuria (2100ml from 3600ml/day). My question was really of academic interest, if the mentioned data allow to exclude primary polydipsia (as a cause of free-electrolyte water - 1500ml from 3600ml) without using water deprivation test and if allow to confirm more likely cause of free electrolyte water loss - the decreased concentration ability. I agree that the primary polydipsia is unlikely.
Maybe my question is hard to understand because I'm missing something.
But I can not agree with dr. Brivet that primary polydipsia is not associated with hyponatremia, although the mechanism is unknown.
see: Polydipsia and hyponatremia in psychiatric patients.
Illowsky BP, Kirch DG. Am J Psychiatry. 1988 Jun;145(6):675-83. Review.
In this patient the primary problem is polyuria . Is the polyuria due to water diuresis or solute diuresis . Chronic Interstitial nephritis can produces both nephrogenic diabetes insipidus as well as salt losing nephropathy . The evidence for nephrogenic DI is low urinary Osm , which is partial , as there is improvement with water restriction . The increase in urinary sodium is probably due to correction of hypovolemia , due to salt wasting nephropathy . The hypontremia is probably due to excess water consumption , with restricted salt intake causing hypovolemic hyponatremia . I would treat this patient with salt & water or IV 0.9% Nacl of about 2.5 - 3 litres / day . Francois Brivet used to state that decreased renal function is a sign of volume depletion , even if there are no clinical signs . Whether , this is CKD or AKI or AKI on CKD would be determined by recovery of renal function after correction with saline .
Primary or psychiatric polydipsia may induce hyponatremia , but the prevalence is low , less than one third of patient in two series, in absence of drugs or tumor. Furthermore hyponatremia occurs only in case very important water intake , more than 10 or 15 liters by day and after a long period , time for inappropriate secretion of antidiuretic hormone to occur.
In our ED and ICU, during the last three decades, except one case of status epilepticus secondary to CNS psychiatric drug associated with hyponatremia requiring mechanical ventilation, among all the patients admitted for potomania, hyponatremia was very very rare, I would retrospectively evaluate its prevalence near 5 to 10%, but the potomania was recent and water intake less than 1O liters/d.
Only case reports of hyponatremia associated to potomania are published, thus its real prevalence remains unknown.
This clinical feature should not be confused with the beer potomania characterized excessive Na+ loss due to beer carbohydrates and very low salt intake. A syndrome unknown in Belgium and Germany, since beer is frequently associated with Brezel, a baked bread with an high concentration of NaCl or salted French Fries. In contrast to potomania, beer induced hyponatremia is common in France, particularly in homeless people…
https://www.researchgate.net/publication/6160452_Hyponatremia_Clinical_Diagnosis_and_Management
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