Faint dent in OMM smoothly

Aug 6th, 2022
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DocHub is a world-recognized online document editor trusted by millions. It can fulfill almost any user’s request and meets all necessary security and compliance standards to guarantee your data is well protected while modifying your OMM file. Considering its powerful and user-friendly interface offered at a reasonable price, DocHub is one of the most winning choices out there for optimized document management.

Five steps to Faint dent in OMM with DocHub:

  1. Upload your file to our editor. Choose how you prefer - dragging and dropping it into our uploading pane, browsing from your device, the cloud, or via a secure URL to a third-party resource.
  2. Start editing your OMM file. Use our tool pane above to add and edit text, or insert images, lines, symbols, and comments.
  3. Make more alterations to your work. Turn your OMM document into a fillable form with fields for text, dropdowns, initials, dates, and signatures.
  4. Add legally-binding eSignatures. Create your valid eSignature by clicking on the Sign button above and assign Signature Fields to all the other people involved.
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How to Faint dent in OMM

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Dent disease type 1 is caused by changes (mutations) in the CLCN5 gene. Dent disease type 2 is caused by mutations in the OCRL1 gene. Both of these genes are located on the X chromosome. These mutations may be inherited or occur randomly with no previous family history of the disorder (spontaneously).
Dents disease is a genetic disorder caused by mutations in the gene CLCN5, which encodes a kidney-specific voltage-gated chloride channel, a 746-amino-acid protein (CLC-5) with 12 to 13 transmembrane domains.
Clinical characteristics. Thirty to 80% of affected males develop end-stage renal disease (ESRD) between ages 30 and 50 years; in some instances ESRD does not develop until the sixth decade of life or later. The disease may also be accompanied by rickets or osteomalacia, growth restriction, and short stature.
Some people with Dent disease develop rickets , a bone disorder that results when the levels of vitamin D and certain minerals (including calcium) in the blood become too low. Rickets can be associated with weakening and softening of the bones, bone pain, bowed legs, and difficulty walking.
Dent disease type 1 is an X-linked recessive renal tubular disease that classically manifests with low molecular weight proteinuria (LMWP), hypercalciuria leading to nephrocalcinosis/nephrolithiasis and one or more additional features like hypophosphatemia, hematuria, bony deformities, short stature and eventually,
The care of patients with Dents disease is supportive, focusing on the treatment of hypercalciuria and the prevention of nephrolithiasis. The vital prognosis is good in the majority of patients. Progression to end-stage renal failure occurs between the 3rd and 5th decades of life in 30-80% of affected males.
A rare genetic renal tubular disease, characterized by manifestations of proximal tubule dysfunction with low-molecular-weight (LMW) proteinuria, hypercalciuria, nephrolithiasis, nephrocalcinosis, and progressive renal failure. Extra-renal involvement is frequent, but may be mild and not recognized.
The most frequent sign of Dent disease is the presence of an abnormally large amount of proteins in the urine (tubular proteinuria). Other common signs of the disorder include excess calcium in the urine (hypercalciuria), calcium deposits in the kidneys (nephrocalcinosis), and kidney stones (nephrolithiasis).

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