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PubMed1999

A paper which changed clinical practice (slowly). Jacob Holler on potassium deficiency in diabetic acidosis (1946).

It is often said that the introduction of insulin into clinical medicine made a 'dramatic' difference to the mortality resulting from diabetic coma. This is true in the sense that before 1922 it was almost uniformly fatal, but until the 1950s the mortality in many large hospitals was as high as 30-50%. Often autopsy did not establish a cause of death. Many may have been a result of hypokalaemia, a complication which was not recognized until 1946; in that year in the Journal of the American Medical Association, Jacob Holler described a patient who developed respiratory paralysis 12h into treatment that, after several hours in an iron lung, was cured by potassium infusion. In the 5 years after Holler's paper there were many reports of deaths resulting from hypokalaemia, as well as several 'near misses', but clinicians were extremely cautious about early replacement probably, as an editorialist in The Lancet suggested, because 'the frightening effects of intravenous injections of potassium made clinicians reluctant to believe in a lack of potassium as a cause of trouble, except in very rare conditions such as familial periodic paralysis'. It had been known since 1923 that insulin lowered serum potassium, but this was not of great interest because the symptoms of hypokalaemia were not known. Also, potassium was not an electrolyte with which clinicians were familiar. Until the introduction of flame photometry in 1950, it was only measured in research studies as chemical methods took several hours to complete.

Diabetic Coma↗
PubMed1978

Effect of potassium deficiency on mouse kidney lysosomal enzymes.

Mice of inbred strains A/J, C57BL/6J and C57BL/6J beige were kept on a K+-deficient diet for up to 40 days to determine the magnitude and mechanism of changes in tissue lysosomal enzymes. From days 10 to 40 glucuronidase activity increased 3-fold in kidney of K+-deficient mice, but there was little effect on beta-galactosidase or acid phosphatase activity. Similar increases in kidney glucuronidase activity occurred in inbred strains known to have genetically altered control of the synthesis (A/J) and secretion (C57BL/6J beige) of glucuronidase in kidney proximal-tubule cells. Deprivation of K+ did not affect glucuronidase activity in liver, spleen, lung and brain, but there was a 2-3-FOld increase in glucuronidase activity in heart in the C57BL/6J and C57BL/6J beige strains. As shown by specific antibody titration, increased glucuronidase activity in kidney of K+-deficient mice was accompanied by accumulation of enzyme molecules. Likewise in kidney of deficient mice there was an increased rate of synthesis of glucuronidase as measured by incorporation of labelled leucine into immunoprecipitable glucuronidase. In kidney of K+-deficient mice the elevated glucuronidase activity was found in both collecting-tubule and interstitial cells of the medulla. It is probable therefore that a significant fraction of the increased kidney lysosomal synthesis and enzyme activity is due to infiltrating cells.

Animals↗
PubMed1992

[The effect of elevated environmental temperature on the development of a potassium deficiency in the body].

Electron microscopy and roentgen microanalysis were used to study the ultrastructure and electrolytic balance of K+, Na+ and Cl- of the animal myocardial tissue during general body hyperthermia. It was established that long-term effect of heating microclimate causes a distinct reduction of K+ in the cardiomyocytes accompanied by essential changes of the ultrastructure of ischemic character.

Animals↗
PubMed1985

Urea reabsorption along the papillary collecting duct in potassium-deficient rats.

These experiments were designed to evaluate the hypothesis that K+ deficiency may be associated with decreased delivery of urea to the renal papillary collecting duct and/or decreased reabsorption of urea from the papillary collecting duct. Either of these factors would result in diminished capacity for urea recycling and might explain the mechanism of the urinary concentrating defect that is observed in K+ depletion. Munich-Wistar rats were fed 25 ml of water and 12 g of normal (CON) or K+-deficient (KD) diet each day for 21 days. Papillary collecting duct samples were obtained by micropuncture through the intact ureter. Fractional delivery of H2O to the base and tip of the papillary collecting duct was increased in KD as compared to CON rats (1.50 +/- 0.30% in KD vs 0.72 +/- 0.09% in CON at the base, P less than 0.01; and 0.55 +/- 0.08% in KD vs 0.30 +/- 0.05% in CON at the tip, P less than 0.01). However, fractional delivery of urea to the base and tip of the papillary collecting duct was not different between KD and CON rats (26.9 +/- 5.6% in KD vs 21.4 +/- 3.3% in CON at the base, P greater than 0.05; and 12.4 +/- 1.5% in KD vs 10.4 +/- 1.4% in CON at the tip, P greater than 0.05). Furthermore, reabsorption of water or urea between the base and tip of the papillary collecting duct was not decreased in KD as compared to CON rats (water reabsorption was 57.8 +/- 4.4% in KD and 55.9 +/- 5.11% in CON and urea reabsorption was 45.0 +/- 6.5% in KD and 45.9 +/- 5.4% in CON, P greater than 0.05). These results demonstrate that water reabsorption, but not urea reabsorption, is impaired in renal tubules proximal to the accessible papillary collecting duct in hydropenic rats.

Absorption↗
PubMedDate not supplied

Paradoxical body and kidney growth in potassium deficiency.

In the growing animal, K deficiency (KD) retards body growth, but paradoxically stimulates renal growth. If KD persists, interstitial infiltrates appear and eventually tubulointerstitial fibrosis develops. In patients with chronic KD, renal cysts may form and with time tubulointerstitial disease with renal failure develops. Since early in KD, kidney IGF-I levels increase and may be a cause of the renal hypertrophy, and as TGF-beta promotes hypertrophy and fibrosis, we examined the expression of these growth factors in chronic KD. Rats were given a KD diet or pair or ad-lib fed a normal K diet. After 21 days, KD rats weighed less than pair fed controls, while the kidneys were 49% larger Serum IGF-I and kidney IGF-I protein levels were depressed, as were IGF-I mRNA levels, and is largely attributable to decreased food intake. Kidney IGFBP-1 and TGF-beta mRNA levels were increased (p < 0.05). There was marked hypertrophy and adenomatous hyperplasia of outer medullary collecting ducts, hypertrophy of thick ascending limbs of Henle (TALH) and interstitial infiltrates. Both nephron segments stained strongly for IGF-I and IGFBP-1. Only the non-hyperplastic TALH was strongly TGF-beta positive. Interstitial infiltrates containing monocytes/macrophages were prominent. These findings are consistent with a sustained role for IGF-I in promoting the renal hypertrophy of KD and appear to be caused by local trapping of IGF-I by the over-expressed IGFBP-1. Localization of TGF-beta to the hypertrophied non-hypoplastic tubules containing IGF-I, suggests that TGF-beta may be acting to convert the proliferative action of IGF-I into a hypertrophic response. TGF-beta may also contribute to the genesis of the tubulointerstitial infiltrate. Finally, the reduced levels of serum IGF-1 levels may be a cause of the blunted body growth.

Angiotensin II↗
PubMed1976

Zonal changes in renal structure and phospholipid metabolism in potassium-deficient rats.

Morphologic alterations and membrane metabolism were studied in the kidneys of rats fed a low potassium diet. Transmission and scanning electron microscopy following perfusion-fixation of kidneys revealed that the earliest morphologic change occurs in cells of the papillary tip in which multivesicular bodies, a specific type to lysosome, appear after 1 day. Increased depletion leads to extension of the lesion to all cells of the papilla. After 1 week, a narrow band of hyperplasia in the inner red medulla appears; this band is characterized by adenomatous proliferation of intercalated and light cells and partial obstruction of collecting tubules. These alterations and cortical growth in the normal pattern result in increased renal weight. New membrane formation for lysosomes and growing cells was studied by measuring the rate of [14C]choline incorporation into phospholipid in slices from five zones of the kidney. In the papilla the rate increased 39 per cent after 18 hours, the earliest change detected. After 36 hours the rate increased in inner red medulla by 28 per cent, inner cortex by 25 per cent and outer cortex by 40 per cent. [14C]choline was a specific precursor of the three renal phospholipids, phosphatidylcholine, lysophosphatidylcholine, and sphingomyelin. The relative distribution of the label did not change with growth induced by potassium depletion. The results indicate that potassium depletion induces early increases in the formation of cell membrane phospholipid which correlate with specific morphologic changes in different zones within the kidney.

Animals↗