Renal supplement Flashcards
What does dark, strong smelling urine indicate?
What does cloudy, pungent urine indicate?
Dark= decreased renal function
cloudy= infectious
What intracellular changes would you expect with polycystic kidney disease?
What does this lead to
- reduction of intracellular calcium and excessive concentrations of cAMP
- normally functioning tissue is slowly reduced as cysts develop of varying sizes
- other organs can develop cysts, especially liver
- decreased GFR and inability to concentrate urine
Where do renal cell carcinomas usually grow?
What are the symptoms?
- Cortex and proximal convoluted tubule
- Usually asymptomatic until advanced
- CVA tenderness, hematuria, palpable mass
What are the stages of RCC?
- stage I- tumor within capsule
- stage II- tumor invades perirenal fat
- stage III- tumor extends into renal vein or regional lymphatics
- IV- metastasis
- lung
- heart
- liver
- other kidney
- bone
What are the different types of renal obstruction?
What are the common causes?
- may be congenical (children) or acquired (adults)
- caused by:
- stones (most common)
- Prostatic hypertrophy
- tumors
- strictures of the ureter or urethra
What are the different classifications of glomerulopathies?
- primary- only the kidney is involved
- secondary- resulting from other disease
- goodpasture syndrome (kidney and lung)
- SLE
- DM neuropathy
- duffuse- all glomeruli
- focal- some but not all glomeruli
- global- affecting all parts of the flomerulus
- segmental- only specific parts/patches
- membranous- thickening of glomerular capillary walls
- sclerotic- scarring
What are some general changes you would see with glomerular disorders?
- hematuria
- proteinuria
- abnormal casts
- decreased GFR
- edema
- hypertension (from inability to properly filter Na and water)
Pathophysiology process of nephrotic syndrom
(chart)
What is membranous nephropathy?
- Immune complexes are deposited on a thickened basement membrane
- this wipes out the foot processes
- The increased thickness of the membrane will cause decreased GFR
- The lack of foot processes will allow proteins through
What are the two different patterns of immune deposition seen in glomerular disorders?
- Circulating (picture on front side)
- immunce complex deposition
- seen in SLE
- the antibodies/complex will be seen in clumps and so will the glomerular damage
- looks “lumpy bumpy” on immunofluoroscence microscopy
- In Situ (picture below)
- caused by an antibody that attaches to a part of the glomerulus, so they are evenly distributed, not in clumps
- Anti-GBM antibody- binds to glomerular basement membrane
- Antibody against glomerular antigen- attaches to foot processes
- looks evenly distributed on immunofluoroscence miscroscopy
- caused by an antibody that attaches to a part of the glomerulus, so they are evenly distributed, not in clumps
How does the basement membrane become damaged in Postinfectious acute glomerulonephritis?
- This usually occurs after some kind on infection (not kidney related)
- the immune system attacks the bacteria and breaks it up into a bunch of little proteins
- as these little proteins go through the kidney, they get stuck in the basement membrane
- these proteins are still a foreign substance, so antibodies (IgG) attach to them and then the immune system goes after them again, this time damaging the basement membrane while doing so.
- sort of autoimmune
What kind of infections are more often followed by postinfectious acute glomerulonephritis?
Where does this usually happen?
Whom does it affect most?
treatment?
- Group A beta-hemolytic streptococci skin and throat infections
- Usually in developing countries
- common in children
- care is supportive- rarely does the kidney become permanently impaired
What is unique about Berger disease?
- It is the only autoimmune disease caused by IgA
- usually IgA antibodies are secreted into the digestive tract, lungs, vagina, etc., but in Berger disease it is found in blood.
- The IgA attaches to the mesangial cells, causing mesangial injury
How does obstruction cause ARF?
- Obstruction distal to the kidney will cause elevated pressure in bowman capsule, impeding filtration
- clinical findings will be based on how long this has been going on for
- prolonged post-renal ARF (obstruction) leats to acute tubular necrosis and if continues will lead to irreversible kidney damage
What are the different phases of post-renal ARF?
- early phase
- afferent arteriole dilates in an attempt to maintain GFR against rising hydrostatic pressure
- lasts 12-24 hours
- late phase
- after 12-24 hrs the afferent dilation ceases, causing progressive fall in renal perfusion and GFR
- may result in anuria
- continues until obstruction is relieved, leading to ischemia and nephron loss
- recovery phase (after obstruction is removed)
- pre-renal vessels relax, perfusion is restored and GFR increases in the surviving nephrons
- tubular pressure returns to normal
- dilation of the calyces and collecting system may remain permanently
What are the two pathophysiological processes of intra-renal problems?
- vascular- renal blood flow is decreased; hypoxia, vasoconstriction
- tubular- inflammation and reperfusion injury, causes casts, obstructs urine flow, tubular backleak
What is the flow chart for acute tubular necrosis, starting with Ischemia and nephrotoxin?
What are the differences in lab values you would expect between pre-renal and intra-renal kidney problems? (table)
FENa%
proteinuria
urine specific gravity
urine osmolality
BUN/Cr ratio
urine Na concentration
urinary sediment
