Renal Flashcards
1/12 people in the US have ___
____ % of all women ages 20-45 will experience a UTI
____ adults over 20 have chronic kidney disease
____ % of kidney failure is caused by diabetes. ____ is the second leading cause of renal failure.
____ people with kidney failure die each year
- Kidney disease is the ___th leading cause of death in America
- There are___ people being kept alive through dialysis
- 1/12 people in the US have renal or urinary tract disease
- 13% of all women ages 20-45 will experience a UTI
- 26 million adults over 20 have chronic kidney disease
- 45% of kidney failure is caused by diabetes. HTN is the 2nd leading cause of renal failure
- Over 87,000 ppl with kidney failure die each year
- Kidney disease is the 9th leading cause of death in US
- 367,000 ppl on dialysis (85 thou waiting for transplant, only 15 thou will get one).
malignant nephrosclerosis (symptoms and treatment)
Azotemia, proteinuria, and further hypertension that the kidney brings on itself
Treatment: anti-hypertensives and dialysis
What is the purpose of autoregulation?
2 mechanisms:
- Maintains constant blood flow to the glomerulus and thus maintain GFR independent of systemic BP.
- Kidneys autoregulate via myogenic mechanism and tubuloglomerular feedback (juxtaglomerular apparatus)
<p>How does sympathetic nervous system affect renin secretion</p>
<p>Increased sympathetic activity --> increased renin release</p>
Symptoms of chronic pyelonephritis
- Chills, fever, headache, general malaise.
- Back pain, tenderness, dysuria, frequency/urgency of urination.
Clear cell carcinoma
- Most common renal tumor in adults.
- Normally asymptomatic due to large renal reserve.
- Symptoms: pain, palpable mass, hematuria
- Called clear cell carcinoma because cells are clear on a stain due to accumulation of lipids
<p>Membranous glomerulonephritis treatment</p>
<p>Steroids for immunomodulation</p>
<p>Focal glomerular disease</p>
<p>Only a few of the glomeruli in a histological section are affected</p>
<p>Minimal change disease treatment</p>
<p>Steroids</p>
<p>Treatment of post-renal ARF</p>
<p>Remove the obstruction</p>
<p>Proteinuria/albuminuria</p>
- protein or albumin in urine
- first indication of glomerular disorder
<p>Diabetic nephropathy</p>
- leading cause of kidney failure!
- 30% of ppl with diabetes (both types) have diabetic nephropathy.
- Treated with ACE inhibitors and angiotensin receptor blockers (ARBs). May require dialysis, though diabetic patients do worse on dialysis than non-diabetic patients.
<p>What is normal GFR</p>
100-125 ml/min.
Declines with age and in pathology.
<p>Anuria</p>
NO urine flow
Local/segmental glomerular disease
A portion of a glomerulus in a histological section is affected
Peritoneal dialysis
- Uses the peritoneal membrane as the semipermeable membrane. By infusing and draining the peritoneal space with dialysis fluid we are able to take waste away without pumping blood in/out of the patient.
- High risk of infection.
Focal segmental glomerulosclerosis histology
Part of the glomerulus shows scarring/sclerosing.
Tons of immunoglobulin present on the side of the glomerulus with sclerosis.
<p>What is BUN &amp; how is it handled by kidney?</p>
Blood urea nitrogen.
Urea is filtered and reabsorbed.
<p>Treatment for pre-renal ARF</p>
improve renal perfusion, volume replacement, dialysis
Reversible disease with re-perfusion!
Why has kidney disease risen so rapidly in prevalence in recent years?
OBESITY, HT, Diabetes
Describe the renal vasculature (high level)
1 renal artery enters
1 renal vein exits
NO COLLATERALs
Urolithiasis
Stones found in the urinary tract
Proliferative glomerular disease
Increases cellular glomerulus (more cells present) - could increase number of immune cells in the glomerulus even though they should NOT be present
Chronic glomerulonephritis
- All of the disease progress to this if left untreated.
- The glomeruli solidify partially or wholly, the tubules atrophy, and the arteries show intimal thickening.
- Thin cortex - very small amt of functioning tissue.
- Histology: no Bowman’s space, no open capillaries, solidified and nonfunctional.
What does a BUN/Cr ratio
- Intrarenal ARF.
- Something is wrong with the kidney/tubule; dec in transporter function decreases reabsorb of urea.
Causes of post-renal ARF
Tubular obstruction caused by insult (such as ischemia) –> increase in pressure –> reduced GFR
Where do obstructions occur in post-renal ARF?
- Ureter system - cysts or tumors in abdomen can impinge on lumen of ureters/urethra
- Kidney stones
- Injury to tubule causing dead cells to slough off and obstruct the tubule
Minimal change disease mechanism
Unknown mechanism, but most commonly seen in children following a recent immune response, for example in illness or with a vaccination.
Membranous glomerulonephritis histology
Diffuse –> all glomeruli are affected
Increase in extracellular substances (thickened capillary loops)
IgA Nephropathy (Berger)
- After a mucosal infection large amounts of IgA antibodies deposit on the surface of mesangial cells.
- most common glomerular renal disease throughout the world.
- Presents with a slightly thickened basement membrane and large deposits of IgA in the mesangium, causing capillaries to rupture.
- Treat w/ steroids
<p>Most causes of kidney disease are primary or secondary?</p>
<p>secondary</p>
3 mechanisms that affect the renin-angiotensin system (tubuloglomerular feedback)
- Baroreceptors in the afferent arteriole will sense pressure changes (increase in pressure = inhibits renin release)
- Increase in SNS increase renin release
- Macula densa cells in the distal tubule sense flow of NaCl through the DCT and stimulate renin if salt conct is high.
<p>Renin converts \_\_\_ to angiotensin I, which is converted to angiotensin II via \_\_\_.</p>
<p>Angiotensinogen
| ACE</p>
<p>Where does Angiotinsinogen come from? </p>
<p>made continuously in liver</p>
5 functions of angiotensin II:
OVERALL: AngII increase BP through an increase in TPR and BV
- Increase in SNS activity → inc. vasoconstriction and HR
- Inc aldosterone secretion → inc na+ reabsorption → inc water reabsorption → increase BV
- Direct increase in Na/water reabsorption → increase BV
- Promotes vasoconstriction → TPR inc.
- Promote release of ADH → water reabsorption → increase BV
Causes of acute renal failure
Pre-renal: decreased renal perfusion
Intra-renal: Parenchymal renal disease
Post-renal: obstruction to urine flow
Azotemia vs. Uremia
- Azotemia: elevation of BUN and creatinine, related to decreased GFR
- Uremia: manifestations of waste buildup; includes azotemia, acidosis, hyperkalemia (high K+), hypertension, anemia, hypocalcemia (low Ca2+)
<p>Proteinuria/albuminuria:</p>
<p>more than 3 mg of protein in the uriner /day</p>
<p>Hematuria:</p>
<p>blood in the urine</p>
<p>Lipiduria:</p>
<p>lipids in the urine</p>
<p>Oliguria:</p>
<p>decreased urine production</p>
<p>Anuria:</p>
<p> no urine flow</p>
<p>leukocytes in the urine</p>
Pyuria
Chronic Kidney Disease (CKD):
- NOT reversible (acute kidney disease IS reversible!)
- progressive loss of the ability to excrete waste, concentrate urine, and conserve electrolytes.
Diffuse vs. focal
Diffuse – All glomeruli in the field are affected
Focal – only few of the glomeruli are affected
<p>Local/Segmental vs. Global</p>
Local/Segmental – Portion of the glomerulus is affected
Global – Entire glomerulus is affected
<p>Proliferative</p>
Increases in number of cells in the glomerulus
*could be increased number of immune cells in the glomerulus
<p>Membranous</p>
Increase in glomerular basement membrane (not an increase in mesangeal cells).
<p>Necrotizing </p>
Necrosis within glomerulus; death of tissue, build
up of dead tissue
<p>Sclerotic </p>
- Hardening/fibrosis within the glomerulus
- Part or the entire glomerulus will fibrose over with a lot of scar tissue; this will affect the architecture of the glomerular basement membrane.
nephrotic syndrome manifestations:
- edema – low oncotic pressure due to loss of plasma protein
- hypoalbuminemia – loss of protein
- hypercoagulable state – loss of coagulation cascade proteins
- decrease immunoglobulins – prot loss, susceptible to infection.
- Hyperlipoproteinemia
FOCAL and GLOBAL disease
only SOME of the glomeruli in the field are affected BUT for each glomerulus that is affected, the ENTIRE glomerulus will be affected
how do we tell Membranoproliferative Glomerularnephritis from Membranous Glomerularnephritis ?
- in Membranous only GBM thickens
- in Membranoproliferative GBM thickens AND the mesangial cells inc in number (remember proliferative in the name = inc in cell number)
Nephritic syndrome is usually caused by _____
an inflammatory rupture of glomerular capillary
Symptoms of nephritic syndrome
PHAROH
P: proteinuria
H: hematuria
A: azotemia: decrease in renal function leading to an increase in nitrogenous waste products
R: RBC cast in urine
O: Oliguria
H: hypertension because of decrease in renal function (increased blood volume)
Key difference between nephrotic and nephritic syndrome
In nephritic rupture of capillary leads to an increase in proteinuria AND hematuria. In nephrotic only proteinuria.
_____ is the most common glomerular renal disease throughout the world.
IgA Nephropathy
CHRONIC KIDNEY DISEASE
- a progressive loss of kidney SA/loss of nephrons
- decreased ability to excrete waste, concentrate urine and conserve electrolytes
- Causes — Primary CRF (problem within kidney) vs. Secondary CRF (disease outside of kidney causes damage)
Primary Chronic Renal Failure (2 ex)
a problem with the kidney itself
• Chronic glomerulonephritis
• Interstitial nephritis
Secondary Chronic Renal Failure (3 ex)
another pathological problem causes damage to kidney
• Hypertensive vascular disease
• Diabetes
• Partial urinary tract obstruction
Chronic Renal Failure may continue to ____
end-stage renal disease (ESRD)
4 Stages of chronic renal failure
1) Decreased renal reserve - GFR normal, NO effect
2) Renal insufficiency - GFR 20-30%, mild azotemia, nocturia, mild anemia.
3) Renal failure - below 20%, azotemia, acidosis, impaired urine dilution, severe anemia, hypernatremia, hyperkalemia.
4) End Stage RF - GFR below 5%, all organ systems feel the
effects.
at what stage of CRF does a patient needs to start dialysis and be put on the transplant list?
Renal failure – GFR below 20%
Proteinuria leads to…
- decreased immunoglobulin
- hypercoagulable state
- hypoabluminemia (low protein in the blood)
- low protein in blood = decreased oncotic pressure = edema
Pros and Cons of peritoneal dialysis
- Pro – cheaper, more accessible, blood doesnt have to leave body
- Con – not as efficient, needs to be done a lot more, higher risk of infection
Pros and Cons of hemodialysis
- Pro – More efficient, depending on severity may only need a few times a week, lower risk of infection
- Con – more expensive, blood needs to be pumped in and out into a dialyzer through AV fistula, needs to be done at a hospital
Symptoms of uremia
anorexia, nausea, vomiting, diarrhea, weight loss, edema, and neurologic changes
which part of the nephron can we see in the cortex vs. medulla?
cortex – all glomeruli and some proximal and distal convoluted tubule.
Medulla – LOH, and collecting ducts (PCT), more homogenous looking.
podocytes are also known as _____
visceral epithelial cells
GFR is dependent on…
Dependent on oncotic pressure, hydrostatic pressure, and Kf. Major determinant is glomerular capillary pressure (HP)
ESRD counts are highest for ____, but rates are highest for ___, then ___
counts – highest for white
rates – highest for blacks, then native americans.
Acute renal failure is defined as ____, results in an inc in ___.
- a sudden decrease in GFR, resulting in an increase in plasma concentration of waste products (azotemia).
ARF is characterized by: (3)
- Reduced urine = oliguria/anuria
- Retention of water, H+, minerals = metabolic acidosis
- Retention of metabolic waste in blood (BUN, creatinine, etc) = azo
(Sudden loss of renal function causes all of these)
____ almost always evolves in the hospital
Acute renal failure
ARF is divided into three parts:
Pre-Renal (Decreased renal perfusion)
Post-Renal (Obstruction to urine flow)
Parenchymal Renal Disease
Pathogenesis of ARF (what can cause it)
any process that sharply decreases renal perfusion (Low BP):
- Hypotension
- Hypovolemia = volume depletion (fluid loss, bleeding, etc.)
- Primary cardiac pump failure
- Decreased systemic vascular resistance (sepsis = systemic vasodilation)
In Acute Renal failure, how does kidney respond to renal hypoperfusion?
Dec GFR => increase Ang II, ADH, Aldosterone
Result: Na and water retention inc BV and BP
Intrinsic ARF (intrarenal/parenchymal) affects 4 areas of kidney:
Glomerulus
Vessels
Interstitium
Tubules
2 mechanisms of post-renal AFR:
Tubular obstruction – Insult (ischemia) causes cell of the tubules to slough off and a cast within the tubular lumen, leading to a retrograde increase in pressure and reduced GFR.
Tubular backleak– Backward flow of filtrate.
Phases of post-renal ARF:
Early Phase: (lasts only 12–24 hrs) Aff arteriole dilates to inc glomerular perfusion--reflex to maintain GFR despite rising tubular HP. Late Phase: (After 12–24hrs) aff vasodilatation stops. perfusion continues to drop = GFR drop. May have anuria. Phase continues until obstruction is relieved. If prolonged, ischemia leads to permanent nephron loss. Recovery Phase (after relief of urinary obstruction): release of pressure, pre-renal vessels relax, perfusion restored. *Dilatation of calyces, collecting system permanent.*
BUN/Creatinine ratio in prerenal ARF:
Reduced blood flow causes elevated creatinine and BUN. Also, bc tubular flow is slower more BUN reabsorption (more Urea in blood) + more Crt secretion = lower Crt in blood. So ratio INC. >20/1
We see a normal BUN/Creatinine ratio in what kind of ARF? Why?
Post-renal ARF, bc kidney function is normal, problem is AFTER filtration and processing of waste (trouble is getting that filtrate out). Normal ratio = 10-20/1
BUN/Creatinine ratio in intra-renal ARF:
Renal Osteodystrophy caused by ___
Elevated serum phosphate levels
Decreased serum calcium levels
Impaired activation of vitamin D
Hyperparathyriodism
