Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Q: Context: Approximately 12% of bound blood calcium is linked to various anions including phosphate. In patients with end-stage kidney disease (ESKD), serum phosphate is highly variable. We propose that establishing a formula to calculate albumin- and phosphate-corrected total calcium would be more appropriate to estimate free calcium in ESKD patients.', 'In 82 haemodialysis patients, serum ionized calcium (Ca(ion)) and pH were measured by blood gas analyser with ion-selective electrodes at the point-of-care, while bicarbonate, phosphate, albumin, magnesium and total calcium (Ca(tot)) were measured at the central laboratory. Linear regression analysis of measured variables was used to best fit adjusted calcium versus Ca(ion).', 'The most parsimonious multiple linear regression model (r(2) = 0.81) of variables associated with Ca(ion) included Ca(tot) (coeff 0.820, P < 0.0001), albumin (coeff -0.016, P < 0.0001) and phosphate (coeff -0.063, P < 0.002). Modelling of available variables yielded the following equation to adjust calcium for albumin and phosphate: Ca(albPh) = Ca(tot) + (0.015 x (40 - [albumin]) + 0.07 x (1.5 - [phosphate])). At an ambient albumin of 40 g/L, Ca(albPh) would be 0.07 mmol/L lower than Ca(tot) for every mmol/L of phosphate. In vitro data using three different albumin levels and increasing phosphate concentrations demonstrated this relationship, with the slope of the phosphate effect being stronger at lower albumin concentrations.
Answer: Because guidelines recommendations indicate that corrected serum calcium should be maintained within the normal range in ESKD patients, inclusion of phosphate to correct Ca(tot) in these patients may have clinical implications on the choice of phosphate binders and the prescription of vitamin D or calcimimetic agents.

A: Is serum phosphate an important determinant of corrected serum calcium in end-stage kidney disease?
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Q: Context: Despite advances in the diagnosis and management of idiopathic noncirrhotic portal hypertension, its pathogenesis remains elusive. Insight may be gained from study of early-onset familial idiopathic noncirrhotic portal hypertension, in which Mendelian mutations may account for disease. We performed exome sequencing of eight subjects from six kindreds with onset of portal hypertension of indeterminate etiology during infancy or childhood. Three subjects from two consanguineous families shared the identical rare homozygous p.N46S mutation in DGUOK, a deoxyguanosine kinase required for mitochondrial DNA replication; haplotype sharing demonstrated that the mutation in the two families was inherited from a remote common ancestor. All three affected subjects had stable portal hypertension with noncirrhotic liver disease for 6-16 years of follow-up. This mutation impairs adenosine triphosphate binding and reduces catalytic activity. Loss-of-function mutations in DGUOK have previously been implicated in cirrhosis and liver failure but not in isolated portal hypertension. Interestingly, treatment of patients with human immunodeficiency viral infection with the nucleoside analogue didanosine is known to cause portal hypertension in a subset of patients and lowers deoxyguanosine kinase levels in vitro; the current findings implicate these effects on deoxyguanosine kinase in the causal mechanism.
Answer: Our findings provide new insight into the mechanisms mediating inherited and acquired noncirrhotic portal hypertension, expand the phenotypic spectrum of DGUOK deficiency, and provide a new genetic test for a specific cause of idiopathic noncirrhotic portal hypertension. (Hepatology 2016;63:1977-1986).

A: Does recurrent recessive mutation in deoxyguanosine kinase cause idiopathic noncirrhotic portal hypertension?
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Q: Context: A retrospective study on patients with chronic nonspecific low back pain (NSLBP).', 'To describe the gait stride characteristics of patients with chronic NSLBP, and to examine the effect of a novel biomechanical device on the gait stride characteristics of these patients.', 'Patient with NSLBP alters their gait patterns. This is considered a protective mechanism as patients try to avoid extensive hip and spine ranges of motion and minimize forces and moments acting on the body. In addition, there are changes in the neuromuscular control system in patients with LBP that could possibly be attributed to the effects of pain on motor control.', 'Nineteen patients underwent a gait test, using an electronic walkway, at baseline and after 12 weeks of treatment. Spatiotemporal parameters were used to identify changes in gait pattern. A novel biomechanical device comprised of 4 modular elements attached to foot-worn platforms was used in the study. The modules are 2 convex shaped biomechanical elements attached to each foot, one is located under the hindfoot region and the other is located under the forefoot region. The device was individually calibrated to each patient. The patients were instructed to walk with the calibrated biomechanical device on a daily basis for a period of 12 weeks.', 'Significant differences were found at baseline and after 12 weeks in normalized velocity (P = 0.03), cadence (P < 0.01), left normalized step length (P = 0.02), right normalized step length (P = 0.02), right swing (P < 0.01), right stance (P < 0.01), left single limb support (P = 0.01), left double limb support (P = 0.02), and right double limb support (P = 0.02).
Answer: Patients with NSLBP treated with the novel biomechanical device for 3 months increased walking speed through longer step length and eliminated asymmetrical differences.

A:
Does a novel biomechanical device improve gait pattern in patient with chronic nonspecific low back pain?
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