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Biomedical subjects

J C Mackenzie

Publications and source records attributed to J C Mackenzie.

At least 19 recordsLinked to original sources
PubMed1993

Treatment of hypercalcaemia with pamidronate in patients with end stage renal failure.

Pamidronate was given to 10 patients with end stage renal failure who had become symptomatically hypercalcaemic due to the use of calcium based phosphate binders and alphacalcidol. All patients were initially treated with rehydration, increased dialysis and withdrawal of drugs, however despite this they remained symptomatic and the serum calcium remained elevated, mean 3.89 mmol/l (range 3.44-4.74). Pamidronate was given, and the serum calcium had declined to 2.92 mmol/l (2.79-3.84), p < 0.01 by the third day. The reduction in serum calcium observed with pamidronate was more rapid than that in 9 patients who developed asymptomatic hypercalcaemia, mean serum calcium 3.45 mmol/l (3.4-3.56), with an actual median reduction of 0.72 mmol/l (0.37-1.30) in the pamidronate group after 3 days compared to 0.20 mmol/l (0.10-0.52) in the conservatively treated asymptomatic group, p < 0.01, and a median percentage decrease of 19% (10-30) in the pamidronate group and 6% (3-15) in the asymptomatic group, p < 0.01. In this study pamidronate was a safe and effective agent in reducing serum calcium in a group of hypercalcaemic dialysis patients.

Calcium Carbonate↗
PubMed1993

Thyroid hormone levels in acute renal failure.

We investigated the plasma concentrations of thyroid hormones in 27 patients with acute renal failure. Both the mean free T3, 1.17 +/- 0.74(SD) pmol/L (range 0.5-2.9 pmol/L) and total T3 plasma concentrations, 0.43 +/- 0.14 nmol/L (range 0.3-0.7 nmol/L) were reduced compared to the normal range (3.3-8.2 pmol/L and 1.0-3.0 nmol/L, respectively). In all 15 patients with plasma creatinine > 3.33 mg/dL (295 mumol/L), the mean FT3 was 0.92 pmol/L and the plasma concentrations have all been < 1.5 pmol/L. There was a weak correlation between the plasma creatinine and the plasma concentrations of TT3 (r = 0.38, p = 0.049). Similarly, both plasma free T4 and total T4 were also reduced in the patients compared to the normal range: mean free T4 5.91 +/- 3.68 pmol/L, range 1.0-13.1 pmol/L, and total T4 47.80 +/- 29.31 nmol/L, range 5-99 nmol/L; normal range 9.4-25.0 pmol/L and 50-160 nmol/L, respectively. There was no difference between the ranges in either plasma TSH, patients 1.19 +/- 1.25 mU/L, range 0.1-4.9 mU/L, vs. control range 0.3-6.0 mU/L; and TBG, patients 19.05 mg/L +/- 3.69, range 11.0-26.9 mg/L, controls range 13.0-30.0 mg/L. Thus we have determined that patients in the early phase of ARF have consistently reduced plasma concentrations of both free and total T3, and reduced concentrations of free and total T4; and that the reduction of TT3 is dependent upon the plasma creatinine level.

Acute Kidney Injury↗
PubMed1992

Neurotoxicity of acyclovir in patients with end-stage renal failure treated with continuous ambulatory peritoneal dialysis.

We report two cases of herpes-zoster in which the administration of acyclovir to patients with end-stage renal failure treated by continuous ambulatory peritoneal dialysis (CAPD) resulted in acyclovir neurotoxicity, even though the doses administered were within those recommended by the manufacturer's data sheet for patients with renal failure. Acyclovir removal was negligible with peritoneal dialysis and one patient died. The other patient was successfully treated with hemodialysis, which effectively reduced plasma concentrations, resulting in an improvement in conscious state. Acyclovir neurotoxicity should be considered in patients with renal failure who have been treated for viral infections, in whom the conscious state has deteriorated despite normal brain computed tomography (CT) scan and lumbar puncture investigations. Hemodialysis is the preferred treatment for the rapid removal of acyclovir.

Acyclovir↗
PubMed1992

A peptide family being re-united: the angiotensins coming in from the cold.

The renin-angiotensin-aldosterone system is now considered to be far more complex than previously thought when the vasoconstrictor and other physiological effects of the octapeptide angiotensin II in the circulating blood were emphasized. The reasons for this altered viewpoint, involving angiotensins other than the octapeptide in the regulation of blood pressure, water and electrolyte homeostasis, are briefly advanced and discussed.

Angiotensin I↗
PubMed1992

An ontogenic study of renal tissue kallikrein in Okamoto spontaneously hypertensive rats: comparisons with human hypertensive nephropathy.

Urinary excretion of tissue kallikrein is reduced in essential hypertension. Although a similar finding has been reported in spontaneously hypertensive rats (SHR), only a few studies have been concerned with the amount of enzyme within the kidney both at the time of onset and during progression of the hypertension. We have performed an ontogenic study on the renal parenchymal values and immunoreactivity of tissue kallikrein in Okamoto SHR aged 4-78 weeks. Additionally, these two parameters were analysed in human biopsies taken from patients with hypertensive nephropathy. The enzymatic activity of renal tissue kallikrein (active and total; specifically antagonized by anti-tissue kallikrein antibodies), increased from 4 to 52 weeks in SHR when compared to normotensive Wistar Kyoto (WKY) rats; this increase was associated with a significant increase in blood pressure. In contrast, 78 weeks SHR and human biopsy tissue showed a substantial reduction in tissue kallikrein values. Also, both renal tissues showed a reduction in immunoreactivity in the cells of the connecting tubules that specifically store the enzyme. In advanced hypertension the observed reduction in tissue kallikrein was probably secondary to a loss of distal tubular mass, as a result of tubular atrophy and fibrosis. The greater values for renal tissue kallikrein in the kidney and reported reduced urinary excretion during the early phases of spontaneous hypertension may be explained by a primary defect in the mechanisms that regulate release of tissue kallikrein from the connecting tubule cells.

Animals↗
PubMed1992

C1q nephropathy: do C1q deposits have any prognostic significance in the nephrotic syndrome?

C1q deposits are usually found in association with other complement components and immunoglobulins in proliferative glomerulonephritis and may predominate in systemic lupus erythematosus (SLE). We report the clinical outcome of four patients who developed a nephrotic syndrome associated with C1q nephropathy unrelated to SLE. On presentation the mean urinary protein loss was 6.8 g/24 h (range 4-10), and renal function impaired, mean serum creatinine 201 mumol/l (150-400). Over a mean follow up period of 6.5 years (1.7-19), all four patients improved, three spontaneously and one treated with steroids and cyclosporin, to a current urinary protein loss of 0.3 g/24 h (less than 0.2-0.9) and serum creatinine 98 mumol/l (68-115). C1q nephropathy was confirmed in each biopsy by conventional immunohistology. C1q deposits were demonstrated within the glomerular basement membrane of three biopsies and the mesangium in two samples. One patient had been categorized on light- and electron-microscopy as having mesangiocapillary glomerulonephritis, one membranous glomerulonephritis, one proliferative glomerulonephritis with focal segmental glomerulosclerosis, and one diffuse proliferative glomerulonephritis with both subendothelial and mesangial dense deposits. In view of the expected progressive nature of the underlying renal histopathological appearance, the presence of predominant C1q deposits would appear to be associated with a better clinical outcome.

Adult↗
PubMed1991

Twenty years of investigating angiotensin activity: an overview.

A short account of the renin-angiotensin-aldosterone system is given with emphasis on the relationship between the octapeptide angiotensin II and its decapeptide precursor angiotensin I. Although the decapeptide is generally assumed to have no biological activity, extensive investigations have indicated that such an assumption is almost certainly unjustified. The implications of the findings are briefly outlined and discussed.

Angiotensin I↗
PubMed1990

Cellular localisation of atrial natriuretic factor in the human kidney.

We have localised atrial natriuretic factor (ANF) in the human kidney by immunocytochemistry and radioimmunoassay. ANF is specifically visualised in the distal convoluted tubule cells and the intercalated cells of the connecting tubules and collecting ducts of the human nephron. The number of immunoreactive cells and tissue values for the peptide were compared between samples from normal kidneys and biopsies obtained from hypertensive patients, in whom the tissue ANF immunoreactivity was found to be reduced. Specific experiments are necessary to establish whether renal ANF is synthesised de novo or captured through endocytosis by the renal tubular cells. The possible functional roles of renal ANF are discussed.

Aged↗
PubMed1990

Electrolyte and humoral responses of renal transplant patients to head-out water immersion.

Eighteen renal transplant recipients and sixteen volunteers were subjected to the physiological manoeuvre of head-out water immersion, in order to compare changes in electrolyte and humoral responses known to occur in healthy individuals with those arising as a result of renal denervation in the transplant recipients. Although the tubular sodium response to water immersion was normal, tubular potassium excretion was markedly different in the transplant patients. Plasma values of atrial natriuretic factor increased in both groups and showed a close temporal relationship to urinary excretion of cyclic GMP. The attenuation in transplant recipients of the well-documented suppression of plasma renin activity during water immersion was probably due to a combination of factors, namely lack of renal innervation and an increase in circulating ANF. The small but significant increase in the excretion of enzymically active urinary kallikrein observed only in the transplant recipients during immersion still requires explanation.

Adult↗
PubMed1989

Presence of immunoreactive tissue kallikrein in human polymorphonuclear (PMN) leucocytes.

The presence of tissue kallikrein in polymorphonuclear (PMN) leucocytes from normal human blood and from patients with rheumatoid arthritis and pyelonephritis was investigated. Immunoreactive tissue kallikrein was specifically detected in neutrophil leucocytes. PMN leucocytes displayed a granular staining. In the synovial membrane and kidney, the cells were aggregated into pockets as part of an inflammatory infiltrate. The presence of immunoreactive tissue kallikrein in human PMN leucocytes may provide a new insight into the importance of this enzyme in inflammation.

Arthritis, Rheumatoid↗
PubMed1988

Localisation of immunoreactive kininogen and tissue kallikrein in the human nephron.

The cellular localisation of kininogen and its relationships with tissue kallikrein containing cells was studied in the human kidney by the peroxidase-antiperoxidase method using antisera to human LMW kininogen and to human tissue kallikrein. Immunoreactive kininogen was localised in the principal cells of collecting ducts. Immunoreactive tissue kallikrein was detected in the connecting tubule cells, segment of the nephron preceding the cortical collecting ducts. The co-existence of tissue kallikrein and kininogen in the same transitional tubule, but in different cells, was established by the use of serial sections and double immunostaining. This anatomical relationship is in accordance with known studies that describe intermingling of principal cells and connecting tubule cells where connecting tubules merge into cortical collecting ducts in the human nephron. The close relationship between cells that contain tissue kallikrein and its substrate, kininogen, suggests that kinins could be generated in the lumen of distal cortical segments of the human nephron.

Humans↗
PubMed1987

Do angiotensin-induced changes in sheep renal venous blood and plasma composition indicate a reversal of glomerular filtration?

Angiotensin II markedly lowers the relative cell content of renal venous blood both with injection into the jugular vein and into the left ventricle of anaesthetised sheep; angiotensin I has a similar effect in this regard when given intravenously but the decreased cellular fraction is much less evident with left ventricular injection when the direct presentation to the kidneys precludes prior intra-pulmonary conversion to angiotensin II. The angiotensins also produce readily demonstrable alterations in renal venous plasma electrolyte, protein, creatinine and urea levels. This pattern of changes is related to associated intra-renal haemodynamics, reverse filtration of proximal tubular fluid, a possible anti-diuretic action of angiotensin I itself on the peritubular capillaries and acute renal failure in man and experimental animals.

Angiotensin II↗