However, subsequent studies have found that, though DLD runs in families, it is not usually caused by a mutation in FOXP2 or another specific gene. Current evidence suggests that there are many different genes that can influence language learning, and DLD results when a child inherits a particularly detrimental combination of risk factors, each of which may have only a small effect. Nevertheless, study of the mode of action of the FOXP2 gene has helped identify other common genetic variants involved in the same neural pathways that may play a part in causing DLD.Language disorders are associated with aspects of home environment, and it is often assumed that this is a causal link, with poor language stimulation leading to weak language skills. Twin studies, however, show that two children in the same home environment can have very different language outcomes, suggesting we should consider other explanations for the link. Children with DLD often grow up into adults who have relatively low educational attainments, and their children may share a genetic risk for language disorder.One non-genetic factor that is known to have a specific impact on language development is being a younger sibling in a large family. Associated factors
It has long been noted that males are more affected by DLD than females, with a sex ratio of affected males-to-females around 3 or 4:1. However, the sex difference is much less striking in epidemiological samples, suggesting that similar problems may exist in females but are less likely to be detected.
The classic presentation (in 40-50% of the cases) is episodic frank hematuria which usually starts within a day or two of a non-specific upper respiratory tract infection (hence synpharyngitic) as opposed to post-streptococcal glomerulonephritis which occurs some time (weeks) after initial infection. Less commonly gastrointestinal or urinary infection can be the inciting agent. All of these infections have in common the activation of mucosal defenses and hence IgA antibody production. Iodinated contrast media
Kidney disease induced by iodinated contrast media (ICM) is called CIN (= contrast induced nephropathy) or contrast-induced AKI (= acute kidney injury). Currently, the underlying mechanisms are unclear. But there is a body of evidence that several factors including apoptosis-induction seem to play a role. Lithium
Lithium, a medication commonly used to treat bipolar disorder and schizoaffective disorders, can cause nephrogenic diabetes insipidus; its long-term use can lead to nephropathy. Lupus
Despite expensive treatments, lupus nephritis remains a major cause of morbidity and mortality in people with relapsing or refractory lupus nephritis. Xanthine oxidase deficiency
Another possible cause of Kidney disease is due to decreased function of xanthine oxidase in the purine degradation pathway. Xanthine oxidase will degrade hypoxanthine to xanthine and then to uric acid. Xanthine is not very soluble in water; therefore, an increase in xanthine forms crystals (which can lead to kidney stones) and result in damage to the kidney. Xanthine oxidase inhibitors, like allopurinol, can cause nephropathy. Polycystic disease of the kidneys
Additional possible cause of nephropathy is due to the formation of cysts or pockets containing fluid within the kidneys.