Hypomagnesemia due to renal disease of unknown etiology

Runeberg, L; Collan, Yrjö; Jokinen, E. J.; Lähdevirta, Juhani; Aro, Antti

doi:10.1016/0002-9343(75)90481-7

Cited by 55 publications

(24 citation statements)

References 16 publications

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“…with oral water rather than with intravenous hypotonic infusion) as that performed by others, whose results in controls and patients were similar to ours [3. 5, 6, 12], There were no features, such as nephrocalcinosis, hypercalciuria and renal insufficiency, which were associated with renal Mg and K wasting in some patients [26,27], who were believed to have differ ent syndromes than BS [28]. Although Mg depletion may be associated with hyperaldosteronism and renal K wast ing [29], this was an unlikely explanation for the clinical picture in our patients since hypomagnesemia was of mild degree in all affected patients, and in none it was lower than 0.41 mM (1 mg/dl), which is considered a threshold limit for symptomaticity [29]; moreover, patient 4, who was not hypomagnesemic, had a similar clinical and bio chemical pattern as hypomagnesemic patients.…”

Section: Discussionmentioning

confidence: 99%

Distal Nephron Function in Bartter’s Syndrome: Abnormal Conductance to Chloride in the Cortical Collecting Tubule?

Colussi

Rombolà²,

Verde³

et al. 1992

Am J Nephrol

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Five patients with the clinical patterns of Bartter’s syndrome underwent a series of clearance studies in order to characterize the underlying tubule defect. Free water generation during maximal water diuresis (Ch₂o), expressed as percentage of the distal delivery (Ch₂o + C_cl), was lower in the patients (72.5 ± 3.2%) than in controls (84.4 ± 5.5, p < 0.0001). During maximal water diuresis and furosemide administration (40 mg i.v. as bolus), NaCl reabsorption along the diluting nephron segments could be separated into 2 components, that occurring in the loop of Henle (DR_NaHL) and that occurring in tubule segments beyond the macula densa (DR_NaDT): DR_nahl was normal, while DR_NaDT was reduced (3.1 ± 0.8 vs. 6.2 ± 2.5 ml/min in controls, p < 0.015). Thus, according to this furosemide protocol, our patients had normal solute reabsorption in the loop of Henle but reduced NaCl reabsorption in tubule segments beyond the macula densa. During 0.9% saline infusion (2 liters in 2 h, after stimulation of distal Na reabsorption with fludrocortisone) fractional excretion (FE) of K showed a linear rise with the increase of FE_cI.FE_K, however, was much higher in the patients than in controls for every FEci level. In contrast, the infusion of Na₂SO₄, after fludrocortisone administration, induced similar FE_K increases in patients and in controls. Thus, in these patients Na reabsorption in the distal nephron (possibly the cortical collecting tubule) was associated with the generation of a higher than normal electric potential gradient in the presence of CI but not of another poorly reabsorbable anion, such as SO₄^2-. These observations indicate that, in our patients, Henle’s loop function is normal, while the collecting tubule function is abnormal. We suggest that NaCl wasting and enhanced tubular secretion of H⁺ and K in our patients might result from an abnormally low conductance to CI in distal nephron site(s) where Na reabsorption is electrogenic, possibly the cortical collecting tubule. A larger than normal transtubular electric gradient would be generated by Na reabsorption, causing: (1) a direct stimulation of tubular secretion of K and H⁺ (leading to hypokalemia and alkalosis) and (2) inhibition of the reabsorption of Na (‘trapped’ into the tubular lumen by electric forces), with consequent extracellular volume contraction, hyperreninemia and hyperaldosteronism.

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Section: Discussionmentioning

confidence: 99%

Distal Nephron Function in Bartter’s Syndrome: Abnormal Conductance to Chloride in the Cortical Collecting Tubule?

Colussi

Rombolà²,

Verde³

et al. 1992

Am J Nephrol

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“…respect to the latter, there is impressive evidence associating premature, often widespread, CPPD crystal deposition with hyperparathyroidism (13-16), hemochromatosis (13, [17][18][19], hypophosphatasia (13, [20][21][22], and hypomagnesemia (23)(24)(25)(26)(27)(28)(29). A less certain association between oligoarticular chondrocalcinosis and hypothyroidism or myxedema is also suggested (30,31).…”

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confidence: 99%

Inorganic Pyrophosphate in Metabolic Diseases Predisposing to Calcium Pyrophosphate Dihydrate Crystal Deposition

Doherty

Chuck

Hosking

et al. 1991

Arthritis & Rheumatism

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Inorganic pyrophosphate (PP,) levels were estimated by radiometric assay in urine and in synovial fluid (SF) froim asymptomatic, nonarthritic knees of patients with iuntreated metabolic disease and normal controls. SF F'P, was significantly elevated in patients with hyperparathyroidism (mean f SEM 19 k 3 pM; n = 9), hemochromatosis (23 f 5 pM; n = 6), and hypomagnesemia (27 f 0.1 pM; n = 2) compared with normal subjec1.s (10 f 0.5 pM, n = 50), and was low in patients with hypothyroidism (4.2 f 2.3 pM; n = 11) (P < 0.05 all comparisons). Urinary PP, was elevated only in those with hypophosphatasia. Local elevation of ionic PP, may be relevant to the mechanism of crystal formation in metabolic diseases predisposing to calcium pyrophosphate dihydrate (CPPD) crystal deposition. The finding of low SF PP, levels in patients with hypothyroidism further questions the association between this condition and CPPD.Factors recognized as predisposing to chondrocalcinosis due to calcium pyrophosphate dihydrate (CPPD) crystal deposition include aging (M), the osteoarthritis process (2-7), a familial predisposition (1,7-12), and associated metabolic disease (I ,7,13). In

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“…There is no spe cific characteristic likely to separate clearly both entities. Only indirect evidence could suggest the diagnosis of Bartter's syndrome, including in our patient: the lack of correction of hypokalemia despite large magnesium in takes [18,31,[35][36][37], the low distal fractional chloride reabsorption [34], and the PRA and urinary aldosterone excretion remaining unchanged during magnesium re pletion [31,36], However, no one of those arguments is irrefutable.…”

Section: Discussionmentioning

confidence: 97%

“…This fact can be attributed to an improved Na-K-ATPase activity which is known to be magnesium dependent [30], Despite normalization of the magnesium blood con centration and probably the pool after 2 months of large oral magnesium and potassium supplements, the pro found hypokalemia could not be corrected. Tubulopathy with magnesium wasting, beyond the acquired causes [31], is represented by familial magnesium-losing kidney [31][32][33], familial hypokalemic tubulopathy [34,35], and tubulopathy of unknown origin [36], Because often asso ciated with hypokalemia, it can mimic Bartter's syn drome with renal magnesium wasting, making some times the diagnostic approach difficult. There is no spe cific characteristic likely to separate clearly both entities.…”

Section: Discussionmentioning

confidence: 99%

Bartter’s Syndrome with a Salt Reabsorption Defect in the Cortical Part of Henle’s Loop

Soupart

Unger²,

Debieve³

et al. 1988

Am J Nephrol

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The pathogenesis of Bartter’s syndrome remains uncertain. The prevailing theory postulates a defect in salt reabsorption, more frequently described in the thick ascending limb of Henle’s loop. The patient we studied presents a normal urinary concentration capacity associated with impaired dilution, a free water clearance at the lower end of normal (5.4 ml/min/lOOml glomerular filtrate), a decreased distal fractional chloride reabsorption (54%) when studied during hypotonic saline diuresis, and a normal decrease in free water clearance after furosemide (2.1 ml/min/100 ml glomerular filtrate), suggesting a defect in the cortical part of Henle’s loop. When studied during oral water diuresis, the fractional chloride reabsorption was normal (82%). This could be explained by a relative inability of the cortical diluting segment to reach maximal absorptive rates for NaCl. An inappropriate kaliuria related to an excessive delivery of salt load to the distal tubule is suggested by the correlation between urinary potassium and chloride excretion (r = 0.84; p < 0.001). Aldosterone secretion participates also partially in the urinary potassium loss.

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Hypomagnesemia due to renal disease of unknown etiology

Cited by 55 publications

References 16 publications

Distal Nephron Function in Bartter’s Syndrome: Abnormal Conductance to Chloride in the Cortical Collecting Tubule?

Distal Nephron Function in Bartter’s Syndrome: Abnormal Conductance to Chloride in the Cortical Collecting Tubule?

Inorganic Pyrophosphate in Metabolic Diseases Predisposing to Calcium Pyrophosphate Dihydrate Crystal Deposition

Bartter’s Syndrome with a Salt Reabsorption Defect in the Cortical Part of Henle’s Loop

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Hypomagnesemia due to renal disease of unknown etiology

Cited by 55 publications

References 16 publications

Distal Nephron Function in Bartter&rsquo;s Syndrome: Abnormal Conductance to Chloride in the Cortical Collecting Tubule?

Distal Nephron Function in Bartter&rsquo;s Syndrome: Abnormal Conductance to Chloride in the Cortical Collecting Tubule?

Inorganic Pyrophosphate in Metabolic Diseases Predisposing to Calcium Pyrophosphate Dihydrate Crystal Deposition

Bartter&rsquo;s Syndrome with a Salt Reabsorption Defect in the Cortical Part of Henle&rsquo;s Loop

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Distal Nephron Function in Bartter’s Syndrome: Abnormal Conductance to Chloride in the Cortical Collecting Tubule?

Distal Nephron Function in Bartter’s Syndrome: Abnormal Conductance to Chloride in the Cortical Collecting Tubule?

Bartter’s Syndrome with a Salt Reabsorption Defect in the Cortical Part of Henle’s Loop