Tasleem Akhtar ( PMRC Research Centre, Khyber Medical College, Peshawar. )
Zahoor Ullah ( PMRC Research Centre, Khyber Medical College, Peshawar. )
Taslim-ul-Haq ( PMRC Research Centre, Khyber Medical College, Peshawar. )
Sera from seventy uremic patients selected randomly were analysed for their electrolytes (Na+, K + C1 and C02). Marked hyponatremia, hypokalemia and hypochioremia was associated with 51.4,40 and 45.7 percent cases respectively. Fourteen percent cases had serum CO2 concentration above normal showing contraction alkalosis. l.V. fluid used in majority of cases was dextrose in water and combined with the use of diuretic “Lasix” whick may be attributed to the higher percentage of hyponatremia and hypokalemia in this study (JPMA 37: 262, 1987).
Acid, base and electrolyte balance play a vital role in normal cellular function. Adequate functioning of the cells requires not only the delivery of nutrients but also the maintenance of a constant intra and extra cellular environment. The main role of the kidney is the excretion of the waste products of metabolism like urea, creatinine and uric acid and the regulation of the volume and concentration of the various constituents of the body fluids and hence the maintenance of acid, base and electrolyte balance.1
Clinical conditions like uremia which results from direct or indirect interference with kidney functions are accompanied by an imbalance of the acid, base and electrolyte concentrations of body fluid and it is, therefore, impor. tant to monitor and manage these carefully and adequately. In uremia especially gross imbalance occurs because of the wide spread use of plain dextrose for intravenous therapy accompanied by the administration of heavy doses of diuretics like lasix. In our laboratory we have observed sodium levels as low as 101 m.moles/ litre and chloride levels of 32 m.moles/litre. These extremely abnormal results prompted us to investigate in detail the current management of cases of uremia in various medical and surgical units of the two teaching hospitals. Any deficiency in the management reported in this paper are primarily owing to a lack of adequate laboratory facilities round the clock and consequent incapability on the part of the clinicians to monitor the electrolyte levels.
MATERIAL AND METhOD
A total of 70 cases, 52 (743%) males and 18 (25.7%) females, having blood urea more than 80 mg/lOOml with various types of renal failures referred from medical and surgical units of both Khyber and Lady Reading Hospitals, Peshawar were included in this study.
Information about primary diagnosis, duration of illness, type and volume of intravenous fluid administered, type and dose of diuretic therapy given and dietary histories about salts restriction were recorded on a standard proforma.
Four to five mls of plain blood samples were taken for serum electrolytes estimation.
Serum sodium and potassium were determined using emission flame photometry with Gallenkamp flame analyser.
Serum chloride was estimated titremetrically2 and total CO2 with Harleco micro CO2 appaEatus 64987.
The high percentage of hyponatremia and hypokalemia may be due to the common practice of administering I.V. dextrose in water which although is isotonic but leaves water only when glucose is metabolised. When very much water is retained, plasma (Na+) falls because:
Variable degree of salt wasting due to reduced sodium chloride reabsorption are present in a variety of renal diseases. Most patients with renal insufficiency are unable to maximally conserve sodium if placed on a sodium restricted diet, as are in this study (64.2%); in contrast, normal subjects can lower Nat excretion to less than 5 m.moles/day. A patient with renal disease may have an obligatory Na+ loss of 10-40 m.moles/ day.3
The decrease in Nat reabsorption appears also to be due to in part to the osmotic diuresis as a result of increased urea excretion in the remaining functioning nephron4
This degree of Nat wasting usually is not clinically important since normal sodium balance is maintained as long as the patient is on a regular diet.
However a low sodium diet is potentially hazardous and should be prescribed only with careful monitoring of the patient.
In rare cases, the patient showed a more severe degree of Nat wasting and hypovolemia will ensue unless the patient maintains a high sodium intake. This occurs primarily in tubular and interstitial disease such as medulary cystic disease, chronic pyelonephritis, polycystic renal disease, the diuretic phase of acute tubular necrosis and after the release of urinary tract obstruction5-8
In these conditions the tubular epithelium is damaged resulting in a fall in Na+ reabsorption and obligatory urinary losses that may be greater than 100 m.moles/day. It is therefore suggested that therapy must be directed towards finding the level of Na+ balance and enough Nat must be given to replace obligatory urine losses.
However it should not be assumed that a patient with salt wasting has a normal ability to excrete a Na+ load because some patients with renal failure develop volume depletion with Na+ restriction, may develop Nat retention, odema and hypertension if placed on a diet rich in Nat. In such patients the range of Na+ balance is relatively narrow and must be determined empirically.
Salt wasting nephropathies may also be complicated by hypoka.lemia and hyperkalemia as 39 and 11.4% of cases in the present study has been found (Table IV).
If the impairment in tubular reabsorption occurs in the proximal tubule or loop of Henle, there will be an increase in K+ and water delivery to K+ excretory site in the distal tubule resulting in enhanced K secretion and possibly K+deple tion and hypokalemia. In severe cases daily K+ losses in the urine can exceed 200 L9 m.moles . However if volume depletion develops because of lack of replacement of urinary Na+ losses, there may be a decrease in renal perfuion thereby reducing K+ excretion and predisposing towards hyperkalemia.
Table V shows that 45% of cases are hypochioremic out of which almost 50% have severe hypochioremia which is a common condition after persistent vomiting, severe burns, diarrhoea, “Salt loss kidney”, uremia and Addison’s Disease.
Chloride concentration is markedly affected by changes in Na+ concentration . In hyponatremia the chloride figure is usually reduced by a similar amount unless ther are also disturbances of acid base balance which affects the HCO3 concentration. Very low figures for chloride down to 50 m.moles/litre have been reported to be associated with marked hyponatremia1 and in this study 4.3% cases have been noted with serum chloride concentration below 60 m.moles/litre.
When the body is depleted of chloride serum HCO3 concentration increases to maintain an ion concentration.
If table V and VI are compared it can be seen that the 11.4% of markedly hypochioremic cases are counter balanced by 14.2% cases having serum CO2 level significantly elevated, leading to Alkalosis. In such cases, beside the removal of hypovolemia, check should also be kept on electrolytes level and especially when only dextrose in water is administered which, after the glucose being metabolized, leaves only water, which if retained lowers the plasma Na and K+ level considerably. Also, when diuretics are used with dextrose in water I.V. therapy, the check on electrolytes level becomes very much essential.
Lasix which is a more active of diuretics and commonly used (in 81.7% cases in the study under report), acts on the ascending limb of the loot of Henle. It causes excessive diuresis and Na and K+ loss.
Thanks are due to Consultant Surgeons and Physicians of all units of both Khyber and Lady Reading Hospitals Peshawar especially to Prof. Tariq Nishtar for referring their cases. Dr Tasleem Akhtar is greatly acknowledged for her valuable suggestions and guidance and Mr. Mohammad Zaid and Wisal Klian Laboratory Assistants and Mr. Mohammad Hayat for their assistance and typing the manuscript.
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