When there is increased calcium present within the kidney it can either lead to?
nephrocalcinosis or nephrolithiasis
generalized calcification which can result from either of the two fundamental types of pathologic calcification: metastatic or dystrophic
Nephrocalcinosis can involve either the (1) or the (2)
1. tubules 2. interstitial area between tubular cells
Nephrocalcinosis leads to the destruction of the tubular system, resulting in reduced (1), (2) (loss of sodium), or (3) (loss of bicarb or retention of acid as H+).
1. renal concentrating ability 2. salt wasting 3. renal tubular acidosis
Metastatic calcification usually present when there is (1), caused by such disorders as (2), or (3) which increase calcium; or disorders that increase intestinal calcium absorption, like (4)
1. elevated serum calcium 2. primary hyperparathyroidism 3. osteolytic cancer metastasis 4. vitamin D overdose or sarcoidosis
Nephrocalcinosis from metastatic calcification consists of wedge shaped scars which microscopically show calcification within (1) as well as the (2)
1. tubular basement membrane 2. interstitium
Ultrastructurally (electron microscopy), the calcium is present within (1)
Nephrocalcinosis from metastatic calcification 1. mitochondria
Dystrophic calcification is found in instances where there is (1), and calcification occurs as a result
1. injury or infection
Nephrolithiasis often damage the (1) to cause (2)
1. transitional epithelium 2. hematuria (blood in the urinary tract)
term that refers to intermittent pain
Nephrolithiasis can distend the ureter intermittently, causing ?
In some instances, the stone results from an elevated serum concentration of (1), which directly leads to increased urinary concentration of the insoluble crystals resulting in stone formation
uric acid or cysteine
In the case of the most common type of stones, calcium stones, there is often (1) in the absence of (2)
Another type of calcium stone begins as a (1) stone, which is then surrounded by calcium precipitates as the stone is enlarging
(1) tend to be harder than calcium phosphate stones, and can injure the (2) as they form and pass into the ureter
1. Calcium oxalate stones 2. renal pelvis
Although a bit counterintuitive, (1) can sometimes cause more symptoms because they can pass into the ureters causing pain
Urea splitting bacteria (proteus or providencia) produce (1) stones which are also known as (2). These can be very large stones that form a cast of the (4) and are known as (3) because of their resemblance to deer antlers.
1. magnesium ammonium phosphate 2. struvite 3. staghorn calculi 4. renal pelvis
Uric acid stones form in about one-fifth of patients with (1), but can also be found in patients with (2)
1. hyperuricemia (elevated serum uric acid) 2. normal serum uric acid but elevated uric acid in urine (hyperuricaciduria).
Histologically, there can be yellow streaks as (1) form in the (2) and can lead to tophus formation with (3) surrounding the crystals
1. uric acid crystals 2. renal calyces and pelvis 3. macrophages
There can also be obstruction of more proximal tubules leading into the calyces which can produce dilated tubules
Uric acid stones
Disorders which produce elevated amounts of purines in blood such as the tumor lysis syndrome (when cancer patients have cancer cell lysis from chemotherapy) can lead to?
hyperuricaciduria and uric acid stones
In addition, (1) intoxication due to exposure to metal alloys containing (1) leads to decreased uric acid urinary elimination which can elevate the concentration of uric acid in serum, urine, or both, leading to uric acid stones. This condition is called (2)
1. lead 2. saturnine gout
Histologically there can be yellow streaks as the conditions responsible for stone formation include?
low urine flow, urine pH (some stones form more readily in more acidic and others in more alkaline urine), and super-saturation of the component which forms the crystal.
A relatively common cause of renal stones in children is (1) which results from a mutation in (2)
1. cystinuria 2. the dibasic acid transporter
Cystinuria also causes poor transport of other basic amino acids such as (1) but cysteine is the crystal that forms the stones
1. lysine and arginine
Fanconi’s anemia has a number of abnormalities, including defects in the (1) that can lead to (2)
1. proximal tubule 2. renal tubular acidosis and formation of renal stones
Dent’s disease can result from mutations in specific (1) which leads to increased (2) in urine and ultimately to formation of renal stones
1. chloride channels 2. calcium and phosphate
Less than a quarter of stones occur as a consequence of infections within the (5)
5. renal pelvis or collecting ducts
Nephrocalcinosis effects ____ & ____ causing destruction of the tubular system.
tubules and interstitial area between the tubular cells
Clinical signs of nephrocalcinosis
cause tubular defects aka destruction of the tubular system resulting in: Impaired concentration ability (1st thing lost in renal disease), Salt wasting (loss of sodium) Renal tubular acidosis
•Hypercalcemia (and thus METASTATIC) leading to nephrocalcinosis due to:
•(1) ↑resorption of calcium from bone (various causes)
•(2) ↑Intestinal absorption of calcium (various causes)
•Wedge-shaped scars mixed w/ relatively normal renal tissue.
EM--> nephrocalcinosis, what do you see (be specific)
•MITOCHONDRIA of renal tubular epithelial cells contain abundant calcium deposits.
Smaller stones are MOST HAZARDOUS; why?
•HAZARDOUS—b/c they pass into the ureters and produces colic.
First clinical sign of larger stones
Stones also predispose to ___; both by obstructive nature and by the trauma they produce
_____refers to stones in more downstream parts of the urinary system
Treatment of kidney stones:
1 and 2
Ultrasonic disintegration (lithotripsy) and endoscopic removal
•are hard and sharp --> cause injury to the renal pelvis (so will see hematuria).
Calcium oxalate stones (different lab changes)
- Hypercalcemia AND hypercalciuria (RARE; 5%)
•Most common; 55%; important to check urine!!
3. •Increased uric acid secretion--> _____
Hypercalciuria w/ NO hypercalcemia;
MIXED URIC ACID & CALCIUM STONE
why do you get mixed uric acid and calcium stone?
urate crystals act as nidus around which calcium salts precipitate
_____-->either hereditary (primary ____) or acquired by intestinal overabsorption in pts w/ GI diseases or on vegan diets
•softer and paler due to DYSTROPHIC CALCIFICATION
•Calcium Phosphate Stones
•Elevated serum uric acid due to:
2. Hepatic catabolism of ____ released from ____ of necrotic cells (tumor lysis syndrome—seen with chemotherapy pts + myeloproliferative disorder).
3. Chronic lead intoxication
1. ↑production (gout), ↓excretion.
2. Hepatic catabolism of purines released from DNA of necrotic cells (tumor lysis syndrome—seen with chemotherapy pts + myeloproliferative disorder).
3. Chronic lead intoxication
Chronic lead intoxication interferes w/ ____ by proximal tubules --> uric acid accumulates producing ____
uric acid secretion; saturnine gout
•Stones are smooth, hard, yellow and <2cm.
Uric acid stones are radiolucent
uric acid stone
•Complication of uric acid:
___: uric acid crystal precipitation can obstruct the collecting ducts as a result of increased uric acid concentration in the acidic pH of urine
ARF (Acute Renal Failure)
•Acute urate nephropathy: precipitated uric acid in the collecting ducts is seen grossly as ____.
Tubules ____ to the obstruction are dilated
yellow streaks in the papillae; proximal
•Histology of uric acid:
•____->a focal accumulation of urate crystals surrounded by inflammatory cells (macrophages)
•Urate crystals in the adrenal medulla w/ ____ around them.
____ around the crystals (host response
Gouty tophus; giant cells; Fibrosis
Xanthine Stones: XO deficiency/XO inhibitor (allopurinol and febuxostat
treatment for uric acid stones
____ stones represent a significant proportion of childhood calculi and occur w/ hereditary cystinuria
•Due to mutation in the ____ leads to decreased reabsorption of cystine and other dibasic amino acids (3 things).
dibasic acid transporter; lysine, ornithine, and arginine
•Mutations in SLC 3A1 (recessive)
Mutations in SLC7A9 (dominant)
Congenital mutations in chloride channels --> present w/ kidney stones due to hypercalciuria, aminoaciduria, and phosphaturia
Dent's--> Congenital mutations in chloride channels; present w/ kidney stones due to __, __, and __
hypercalciuria, aminoaciduria, and phosphaturia
Has a number of abnormalities, including defects in energy and certain ion channels in the PROXIMAL TUBULE --> that can lead to renal tubular acidosis and formation of renal stones
Has a number of abnormalities, including defects in energy and certain ion channels in the ___ --> that can lead to ____ and formation of renal stones
PROXIMAL TUBULE; renal tubular acidosis
Urinary loss of AMINO ACIDS, phosphate