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Urinary excretion of excess sulfurous amino acids (e.g., cysteine and methionine), uric acid, and other acidic metabolites from animal protein acidifies the urine, which promotes the formation of kidney stones. [37] Low urinary-citrate excretion is also commonly found in those with a high dietary intake of animal protein, whereas vegetarians ...
A renal diet is a diet aimed at keeping levels of fluids, electrolytes, and minerals balanced in the body in individuals with chronic kidney disease or who are on dialysis. Dietary changes may include the restriction of fluid intake, protein , and electrolytes including sodium , phosphorus , and potassium . [ 1 ]
Diagnosis is based on clinical and laboratory findings of low serum osmolality and low serum sodium. [13] Urinalysis reveals a highly concentrated urine with a high fractional excretion of sodium (high sodium urine content compared to the serum sodium). [14] A suspected diagnosis is based on a serum sodium under 138.
Uric acid displays lactam–lactim tautomerism. [4] Uric acid crystallizes in the lactam form, [5] with computational chemistry also indicating that tautomer to be the most stable. [6] Uric acid is a diprotic acid with pK a1 = 5.4 and pK a2 = 10.3. [7] At physiological pH, urate predominates in solution. [medical citation needed]
The Glomerular filtration rate (GFR) is regarded as the best overall measure of the kidney's ability to carry out these numerous functions. An estimate of the GFR is used clinically to determine the degree of kidney impairment and to track the progression of the disease. The GFR, however, does not reveal the source of the kidney disease.
The disorder is caused by a mutation of the purine nucleoside phosphorylase (PNP) gene, located at chromosome 14q13.1. [3] [4] This mutation was first identified by Eloise Giblett, a professor at the University of Washington, in 1975. [5] PNP is a key enzyme in the purine catabolic [6] pathway, and is required for purine degradation.
In the general population, the frequency of medullary sponge kidney disease is reported to be 0.02–0.005%; that is, 1 in 5000 to 1 in 20,000. The frequency of medullary sponge kidney has been reported by various authors to be 12–21% in patients with kidney stones. [10] The disease is bilateral in 70% of cases. [citation needed]
Unless high blood levels of uric acid are determined in a clinical laboratory, hyperuricemia may not cause noticeable symptoms in most people. [5] Development of gout – which is a painful, short-term disorder – is the most common consequence of hyperuricemia, which causes deposition of uric acid crystals usually in joints of the extremities, but may also induce formation of kidney stones ...