The influence of a cooked-meat meal on estimated glomerular filtration rate.

BACKGROUND: Chronic kidney disease (CKD) is an important but under-recognized condition. Recent national guidelines have recommended that biochemistry laboratories report estimated GFR (eGFR) to improve diagnosis of CKD and facilitate disease staging and management. Previous reports have suggested that intake of large amounts of cooked meat can lead to a significant increase in serum creatinine concentration. METHODS: Participants (n = 32), consisting of 17 healthy volunteers and 15 outpatients, were recruited. Measurement of serum creatinine (kinetic Jaffe method, enzymatic, isotope-dilution mass spectrometry [IDMS]) and cystatin C, and calculation of eGFR were carried out before (i) and after a meal containing cooked meat (ii) and a meat-free meal (iii). RESULTS: Following intake of cooked meat, median serum creatinine concentration (kinetic Jaffe) increased from 80.5 micromol/L preprandially to 101.0 micromol/L 1-2 h postprandially (P<0.0001), and 99.0 micromol/L 3-4 h postprandially (P<0.0001). Median eGFR decreased from 84.0 mL/min/1.73 m2 preprandially to 59.5 mL/min/1.73 m2 1-2 h postprandially (P<0.0001), and 64.0 mL/min/1.73 m2 3-4 h postprandially (P<0.0001). Consumption of non-meat-containing meals had little impact on serum creatinine (kinetic Jaffe) and eGFR. Changes in serum creatinine were similar using all three methods, and cystatin C concentration was generally uninfluenced by food intake. CONCLUSIONS: Intake of cooked meat has a significant effect on serum creatinine concentration and eGFR. Misclassification of CKD is possible if measurements are made after meals containing cooked meat. Clinicians should ensure that CKD classification is based on samples taken in the appropriate conditions: either fasting or after avoidance of cooked meat on the day of sampling. National guidelines which overlook this factor should be revisited.

Serum calcium, urine calcium and polymorphisms of the calcium sensing receptor gene.

BACKGROUND: Recent studies have suggested a correlation between the A986S polymorphism of the calcium sensing receptor (CASR), and serum total and ionized calcium. This study aimed to assess the prevalence of three CASR polymorphisms in a West of Scotland population and relate genotype to serum and urine calcium levels. METHODS: Fasting blood and urine samples were obtained from 121 healthy male and female volunteers aged 20-60 years. Volunteers were genotyped for the A986S, Q1011E and R990G polymorphisms using allele-specific amplification and amplification-created restriction site techniques. Total calcium, ionized calcium and urine calcium excretion were measured using automated clinical chemistry analysers. RESULTS: Genotype frequencies for the A986S polymorphism were: AA, 74.4%; AS, 24.8%; SS, 0.8%. There was a small but statistically significant (P < 0.01) increase in ionized calcium concentration in AS individuals compared with the wild type (1.22 versus 1.20 mmol/L). No statistical difference was detected in serum total calcium or parameters of urine calcium excretion. Genotype frequencies for the remaining polymorphisms were: RR, 82.6%; RG, 16.5%; GG, 0.8% and QQ, 93.4%; QE, 6.6%; EE, 0%. Biochemical parameters in these individuals were not statistically different from the wild type. CONCLUSION: The increase in serum ionized calcium in the AS group was small and, therefore, unlikely to be of clinical significance.

Clinical and laboratory features of calcium-sensing receptor disorders: a systematic review.

Mutations in the calcium-sensing receptor gene (CaSR) may result in disorders of calcium homeostasis manifesting as familial benign hypocalciuric hypercalcaemia (FBHH), neonatal severe hyperparathyroidism (NSHPT) or autosomal dominant hypocalcaemia with hypercalciuria (ADHH). FBHH may have a population prevalence as high as one in 16 000, and ADHH one in 70 000. NSHPT is very rare. The FBHH condition is usually asymptomatic. Parathyroidectomy does not result in normal serum calcium, and no active treatment is indicated. To differentiate FBHH from primary hyperparathyroidism (PHPT), a guideline which includes measurement of serum calcium, intact parathyroid hormone (PTH), magnesium and fasting urinary calcium excretion is proposed. Screening of family members for hypercalcaemia, and occasionally a search for mutations in the CaSR gene, may be required. The NSHPT condition may manifest with hypercalcaemia, (usually) very elevated serum PTH concentration, subperiosteal erosions and fractures. Milder cases may be managed medically, but respiratory failure, extreme hypercalcaemia and failure to thrive are indications for early parathyroidectomy. The ADHH condition may result in asymptomatic hypocalcaemia, but some affected family members have minor symptoms, and a minority experience seizures in infancy which can recur into adulthood. A significant proportion of cases previously reported as idiopathic hypoparathyroidism (IHP) may in fact be due to mutations in the CaSR gene. In a moderately hypocalcaemic patient with no other clearly discernible cause, an elevated urine calcium:creatinine ratio is suggestive of ADHH, as is the presence of a first-degree relative with hypocalcaemia. If treatment with vitamin D analogues is undertaken, serum and urine calcium should be monitored, advice which applies equally to ADHH and IHP.

Iatrogenic copper deficiency causing anaemia and neutropenia.

A 79-year-old woman presented with an obstructed femoral hernia and had a wedge resection of the small intestine. Post-operatively she developed wound dehiscence and spent 3 days in the adult critical care unit. Good recovery followed and she was allowed home after 2 months in hospital. Six months later she presented with anaemia, neutropenia and a very low serum copper concentration. Review of her notes revealed that she had been given oral zinc therapy while in the critical care unit and this treatment had been continued on discharge from hospital. Serum copper, haemoglobin and white cell count recovered after oral zinc was discontinued. Oral zinc treatment can lead to symptomatic copper deficiency in susceptible patients.

Hyperamylasaemia and multiple myeloma.

This case report describes a 42-year-old Caucasian woman who presented with persistent hyperamylasaemia and no evidence of pancreatic pathology. Further investigations resulted in a diagnosis of light-chain multiple myeloma. Amylase production by epithelial tumours has been well documented but the association with multiple myeloma has only been described in a small number of cases. The link does not appear to be immunoglobulin class-specific but the association with Bence Jones myeloma is unusual. The common features in this group of patients have been extensive extramedullary spread with a high tumour mass and a poor prognosis. This case was similar in that the patient showed very rapid disease activity developing extensive metastatic lesions and treatment ultimately proved unsuccessful. The amylase concentrations have been shown to decrease in response to treatment and increase at times of relapse and it has been proposed that it may be useful as a tumour marker in these patients. This case study adds to the pool of patents with this unusual association.