User:Drcheech/sandbox

Possible topics

 * Hypercalciuria (stub/mid)


 * Interstitial nephritis (start/mid)
 * Hemodialysis (C/high)

Article evaluation: "Interstitial Nephritis"

 * Content:
 * Given the significant differences that extend beyond onset/duration of disease itself, it would be helpful to differentiate chronic vs acute TIN in the body of the article, not just intro.
 * Lack of histologic discussion as well as anatomic explanation of the role of the interstitium.
 * List of causes is quite narrow and lacks adequate explanation of pathophysiologic mechanisms of injury.
 * No epidemiologic data.
 * Picture/figure would be nice.
 * Tone:
 * Overall appropriate but could be more academic
 * Sources:
 * The PubMed PMID links seem to all work well.
 * Unfortunately, most of them are primary single study sources rather than secondary sources, reviews, etc.
 * The last resource links did not work so unable to confirm the reliability of this source.
 * Many of the sources are becoming dated.
 * Talk Page:
 * Nada
 * Would be great to restructure the topic per Wiki guidelines for Medicine related articles.

Working Bibliography

 * 1) Meyers CM, Perazella MA. Chapter 44: Chronic Tubulointerstitial Nephritis. NKF Primer on Kidney Disease. 2018.
 * 2) Brewster UC, Lucuano RL. Chapter 33: Acute Interstitial Nephritis. NKF Primer on Kidney Disease. 2018.
 * 3) Alon US. Chapter 44: Pediatric Tubulointerstitial Nephritis. Eds: Avner, Goldstein. Pediatric Nephrology. 2016.
 * 4) Zeisberg M, Kalluri R. Physiology of the Renal Interstitium. CJASN Renal Physiology for the Clinician. 2016.

'Below you will find the entirely new article structure I plan to use (per Wiki guidelines for Medicine related articles). I am filling in edits gradually over time, using the secondary sources which will be continuously updated per the "Working Bibliography" above.'

= Interstitial nephritis = Interstitial nephritis, also known as tubulointerstitial nephritis, is inflammation of the area of the kidney known as the interstitium, which consists of a collection of cells, extracellular matrix, and fluid surrounding the renal tubules. In addition to providing a scaffolding support for the tubular architecture, the interstitium has been shown to participate in the fluid and electrolyte exchange as well as endocrine functions of the kidney. There are a variety of known factors that can provoke the inflammatory process within the renal interstitium, including pharmacologic, environmental, infectious and systemic disease contributors. The spectrum of disease presentation can range from an acute process to a chronic condition with progressive tubular cell damage and renal dysfunction.

Epidemiology
Interstitial nephritis is uncommon (<1% incidence) in patients without any symptoms but occurs in about 10-15% of hospitalized patients with acute kidney injury of unknown cause. While it can occur in patients of all ages, it is more common in elderly patients, perhaps due to increased exposure to drugs and other triggering causes.

Signs and symptoms
Interstitial nephritis may present with a variety of signs and symptoms, many of these nonspecific. Fever is the most common, occurring in 30-50% of patients, particularly those with drug-induced interstitial nephritis. Other general symptoms that occur with variable frequency include nausea, vomiting, fatigue, lack of appetite, and weight loss. More specific symptoms, such as flank pain, pain with urination, and visible blood in the urine, as well as signs like hypertension can be helpful in increasing suspicion for the diagnosis. The "classic" triad of symptoms reported in early documented cases consisted of rash, joint pain, and increased eosinophils in the blood; however, more recent epidemiology suggests that this grouping of symptoms only occurs in a small minority (5-10%) of patients.

Environmental Exposures
(Lead)

Systemic Diseases
(TINU, Immune-mediated, Malignancy)

Pathophysiology
(insert picture)

Pathology
While non-invasive patient evaluation (physical examination, blood and urine testing, imaging studies) can be suggestive, the only way to definitively diagnosis interstitial nephritis is with a tissue diagnosis obtained by kidney biopsy. Pathologic examination will reveal the presence of interstitial edema and inflammatory infiltration with various while blood cells, including neutrophils, eosinophils, and lymphocytes. Generally, blood vessels and glomeruli are not affected. Electron microscopy shows mitochondrial damage in the tubular epithelial cells, vacuoles in the cytoplasm, and enlarged endoplasmic reticulum.

History
(Maybe...)