Case history comments

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Case history comments







Case history 4


These urea and electrolytes are typical of dilutional hyponatraemia. Her normal blood pressure and serum urea and creatinine concentrations make sodium depletion unlikely as the mechanism of her hyponatraemia. The absence of oedema excludes a significant increase in her total body sodium. These results are characteristic of the so-called syndrome of inappropriate antidiuresis (SIAD) and are due to secretion of AVP in response to non-osmotic stimuli. The ectopic production of AVP is extremely rare even in patients with malignant disease. The urine osmolality signifies less than maximally dilute urine, i.e. impaired water excretion, which is in keeping with SIAD. However, it is equally consistent with sodium depletion (the hypovolaemia resulting from sodium and water loss is a powerful non-osmotic stimulus to AVP secretion). In any case, maximally dilute urine (50 mmol/kg or less) is clinically obvious – it is associated with urine flow rates in excess of 500 mL/hour. Thus, measurement of urine osmolality usually adds little to the diagnosis of hyponatraemia.




Case history 6


The biochemical results strongly suggest pre-renal uraemia, as there is a marked increase in the serum urea with a very modest increase in the serum creatinine. He has severe hypernatraemia and these two observations would indicate that the patient is primarily suffering from water depletion. The serum potassium is normal as is his anion gap. These results would, therefore, indicate the presence of profound uncomplicated water depletion.


In cases such as this, it is essential to exclude non-ketotic, diabetic, precoma. His blood glucose was 9.2 mmol/L, which excludes this diagnosis. Ketones were not detected, nor did he have an acidosis. It was rapidly established from the clinical history that the man had not eaten or drunk for more than 3 days. A diagnosis of pure water depletion was therefore established on the basis of the history, clinical findings and biochemical features.




Case history 8


This woman displays features of sodium depletion; she is also likely to have a mild degree of water depletion. The evidence for sodium depletion is her progressive weakness, her pre-renal uraemia and her hyponatraemia. While her glomerular filtration rate has decreased, her tubular function appears satisfactory as demonstrated by her ability to produce a concentrated urine and to conserve her urine sodium. This woman received inadequate intravenous fluid therapy postoperatively. Her treatment regimen was especially deficient in sodium, which led to a contraction of her ECF and this caused her to develop pre-renal uraemia. The contraction in her ECF will also have stimulated AVP secretion and thus she conserved water and became hyponatraemic. The contraction in her ECF also stimulated aldosterone secretion, which caused her renal tubules to conserve sodium.


Ideally, in order to prescribe appropriate fluid therapy for this woman, one needs to estimate her sodium, potassium and water deficits from her fluid balance charts. Particular note must be taken of losses that are relatively rich in sodium, such as drainage fluid, losses from fistulae, stomas or by nasogastric aspiration. Insensible water loss and urinary losses must also be taken into account.



Case history 9


The creatinine clearance is calculated using the formula below where U is the urine creatinine concentration, V is the urine flow-rate and P is the plasma or serum creatinine concentration. As there are 1440 minutes in a day this man’s urine flow-rate, V = 2160/1440 = 1.5 mL/minute. His urinary creatinine must be in the same units as his serum creatinine. His urinary creatinine concentration:


U = 7.5 mmol/L = 7500 µmol/L. His serum creatinine: P = 150 µmol/L. Thus,


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This is low for a young male.


When it was discovered that the urine collection was for 17 hours and not 24 hours, his urine flow-rate was recalculated (2160/1020):


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Recalculating his creatinine clearance:


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This is in the range one would expect in a young male. One can see, therefore, how errors in the timing and collection of urine significantly influence the calculation of the creatinine clearance. Errors in collection are by far the most common and serious errors encountered when estimating the creatinine clearance.







Case history 14


The serum urea in this case, though high, is relatively low in comparison to the serum creatinine. This would be consistent with a low protein intake. The serum bicarbonate is low, indicating the presence of a metabolic acidosis. However, the anion gap is normal and, hence, it is unlikely that this patient’s [H+] will be grossly abnormal. The hyperkalaemia, therefore, is likely to be entirely due to the low glomerular filtration rate with the efflux of potassium from the intracellular to the extracellular compartment being of minor importance. The hyponatraemia in this case reflects impaired water excretion resulting from the inability of the renal tubules to respond to AVP. These results clearly indicate that the patient needs to continue with dialysis. This woman’s serum calcium status should also be assessed. Hypocalcaemia should be excluded and a high serum alkaline phosphatase would indicate the presence of metabolic bone disease. A raised serum PTH concentration is another very sensitive marker of metabolic bone disease in patients with renal failure.


Treatment of metabolic bone disease in renal failure is aimed at correcting hypocalcaemia and hyperphosphataemia, e.g. oral calcium salts and calcitriol (active form of vitamin D).



Case history 15


The low [H+] and high bicarbonate concentration confirm that this patient has a metabolic alkalosis. The raised PCO2 indicates partial respiratory compensation for this. The loss of H+ will have been caused by his severe vomiting which, in view of the history, is likely to be due to pyloric stenosis. Ingestion of bicarbonate would not lead to this degree of metabolic alkalosis though it will have aggravated the situation. The severe vomiting has led to dehydration and this is manifested by the presence of pre-renal uraemia. The hypokalaemia is due to a combination of potassium loss in the vomitus and the metabolic alkalosis causing the influx of potassium from the ECF to the ICF.


The urine results are typical of a patient with dehydration and metabolic alkalosis due to vomiting. Aldosterone is being secreted in an attempt to expand his ECF and the patient is conserving sodium despite his hypernatraemia. The hyperaldosteronism is promoting potassium loss despite hypokalaemia, and hydrogen ion loss, resulting in the classical paradoxical acid urine.





Case history 18


The dominant feature in this patient’s acid–base disorder is an alkalosis as the [H+] is low. The bicarbonate concentration is increased, indicating a metabolic alkalosis. The PCO2 is increased (respiratory acidosis) and this could be due to partial compensation for the metabolic alkalosis. However, the increase in PCO2 is too high for this to be the only explanation. The background history of respiratory disease is the other reason for this patient’s respiratory acidosis.


The PO2 indicates that the patient is satisfactorily oxygenating her blood.


This patient’s hypokalaemia and metabolic alkalosis can be explained by profound potassium depletion due to the use of a diuretic with an inadequate intake of potassium. The principles of therapy are potassium supplementation and alteration of her drug regimen to one that will ameliorate potassium loss, e.g. use of an ACE inhibitor.





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Jun 18, 2016 | Posted by in BIOCHEMISTRY | Comments Off on Case history comments

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