Kidney Function

Crystal-induced kidney disease refers to kidney injury caused by intratubular crystal deposition of calcium salts, medications, or other chemicals. The major risk factors for crystal deposition include hypercalcemia and/or hypercalciuria, hyperoxalosis and/or hyperoxaluria, and increased serum and/or urinary phosphate levels. The risk of crystal-induced kidney disease is increased further in the presence of hypovolemia and urinary concentration, changes in urinary pH, and decrease in level of urinary inhibitors of crystallization, such as citrate, magnesium, and pyrophosphate. In the case of calcium phosphate crystal deposition, use of angiotensin-converting enzyme inhibitors is considered an additional risk factor. In addition to calcium salts and uric acid, drugs such as sulfonamides, foscarnet, methotrexate, triamterene, phosphate-containing bowel preparations, orlistat, ciprofloxacin, and indinavir can cause crystal-induced kidney disease. Clinical manifestations of crystal-induced kidney disease are wide ranging, from no symptoms to flank pain, hematuria, sterile pyuria, crystalluria, and reduced kidney function. Although crystal-induced kidney disease is well documented in native kidneys, its occurrence in kidney allografts is not. We report 2 cases of crystal-induced kidney disease in transplant recipients that resulted in kidney failure.

Calcium is the most abundant element in the human body. 95% of your body’s calcium can be found in your bones and teeth. The second most abundant element in the human body is phosphorus. A large percentage of your body’s phosphorus is combined with the calcium in your skeletal structure. A lesser amount of phosphorus lies in the soft tissues and fluids of your body.

Both calcium and phosphorus are required for the proper formation of bones. The body cannot utilize calcium whatsoever unless active Vitamin D is present. Because non-functioning kidneys cannot activate Vitamin D, calcium from food eaten by someone with non-functioning kidneys cannot be absorbed adequately. Subsequently, your body’s blood calcium level can drop dramatically.

Phosphorus is known to build up in the bodies of patients with non-functioning kidneys which can result in a decrease in the level of blood calcium present. When calcium levels drop, the parathyroid glands secrete the parathyroid hormone which causes calcium to be released from the bones and then sent back into the bloodstream. This release of calcium from your bones may cause them to become weak or brittle, and if this process continues for a prolonged period of time, bones may break.

A doctor monitors this delicate relationship between phosphorus and calcium and may prescribe a calcium supplement. Foods high in phosphorus should be avoided altogether. Additionally, phosphate binders (like calcium salts) may be prescribed in order to prevent the phosphorus in your food from being absorbed into your body.

Why Do I Need to Restrict My Phosphorus Intake?
Due to the fact that high levels of phosphorus in your bloodstream can result in your bones being deprived of much needed calcium, it is of the utmost importance that phosphorus be restricted from your diet. Also, high levels of phosphorus may potentially combine with calcium and deposit in the soft tissues such as your blood vessels, skin, and lungs. If this occurs, you may experience joint pains, itching, and/or eye irritation.

Fanconi syndrome and chronic kidney disease associated with paroxysmal nocturnal hemoglobinuria is rarely reported. We describe a 51-year-old woman with glomerular filtration rate decrease and hypokalemia, glucosuria, and proteinuria during a 4-year period. Paroxysmal nocturnal hemoglobinuria was diagnosed 17 years earlier, and she has received multiple blood transfusions because of hemolytic episodes during the last 5 years. Deteriorating kidney function and persistent Fanconi syndrome were accompanied by a progressive increase in serum ferritin levels. Laboratory studies showed proximal renal tubular acidosis, hypophosphotemic hyperphosphaturia, normoglycemic glucosuria, and aminoaciduria. Serologic testing, tumor markers, Bence-Jones protein, and heavy-metal screening results were negative. Abdominal magnetic resonance imaging showed characteristic features of iron deposition in the bilateral renal cortices. Kidney biopsy showed chronic interstitial nephritis with prominent hemosiderin deposition in the proximal tubules. With potassium citrate, calcitriol, and deferoxamine therapy, Fanconi syndrome persisted, but kidney function was stable. Renal hemosiderosis secondary to both chronic repetitive hemolytic episodes and transfusion-related iron overload in patients with paroxysmal nocturnal hemoglobinuria can lead to Fanconi syndrome and chronic kidney disease.