Renal Disorders Flashcards
Nephrolithiasis is also known as
kidney stones or renal calculi
The presence of renal stones within the renal pelvis and/or calyces is?
Nephrolithiasis
Kidney stones may be present where?
- renal pelvis
- calyces
- ureters
- urinary bladder
The first occurence of kidney stones is usually before the age of?
50
Risk factors for kidney stones are: (10)
- age
- male gender
- fluid intake
- caucasian
- diet
- HTN
- atherosclerosis
- metabolic syndrome
- obesity
- DM type 2
Renal calculi are made up of: (4)
- calcium
- struvite
- uric acid
- cystine
Cystine is?
an amino acid found in most proteins
What are the most common renal calculi made of?
Calcium stones are the most common and are frequently calcium oxalate or calcium phosphate
Why do kidney stones occur?
- idiopathic hypercalciuria
- in the setting of hyperparathyroidism
What results in an increase in osteoclastic activity?
hyperparathyroidism
What are the bone cells which break down bone and release calcium into the blood?
Osteoclasts
What is the second most common type of renal calculi?
Strivite
What is struvite made of?
magnesium, ammonium, and phosphate salts
What causes struvite renal calculi?
They tend to result from chronic UTIs with urease producing bacteria such as proteus and pseudomonas
How are struvite renal calculi produced?
The urease produced by these bacteria breaks down the urea in the urine to the salts that compose struvite stones
What type of renal calculi are the most troubling?
struvite stones
Why are struvite stones the most troubling?
These stones are the most troubling ones because they frequently cause complications with intractable urinary tract infections, pain, bleeding, and abscess.
What is the third most common kidney stone?
Uric acid
How are uric acid stones produced?
Uric acid results from the breakdown of purines (DNA).
Who usually suffers from uric acid kidney stones?
These types of stones tend to form in persons with excess purine intake or persons with gout.
What is the most commonly occuring kidney stone in children?
Cystine stones
What is the least common type of kidney stone for adults?
Cystine stones
What is the pathophysiology of nephrolithiasis?
- begins with the oversaturation of urine with ions (calcium, magnesium, ammonium, etc.)
- The cations and anions bond with one another and form salts which precipitate into crystals.
- The crystals then form stones which pass into the ureter and cause excruciating flank pain (renal colic) and obstruction.
- The obstruction causes the urine to back up into the kidney resulting in hydronephrosis and renal failure.
What size stone will have a 50% chance of passing without any complications?
5mm or less
Stones that are what size will likely not pass spontaneously?
1cm
Specific risk factors for kidney stones: Gout which results from?
an accumulation of uric acid
Specific risk factors for kidney stones: Dehydration…
whose link to the pathophysiology of nephrolithiasis is unknown
Specific risk factors for kidney stones: High protein diets
resulting in an increase in purine intake
Specific risk factors for kidney stones: High sodium diets
predisposes the individual to increased calcium excretion and therefore to calcium stone formation
Specific risk factors for kidney stones: HTN
has a role in the formation of renal calculi but the association is not clear
Clinical manifestations of renal calculi?
- flank pain that radiates to the groin
- anuria (bilateral obstruction)
- azotemia (bilateral obstruction)
- hematuria
Used in medical terminology to refer to a localized area of disease
focal
in relationship to glomerular disorders it means that < 50% of glomeruli are affected by the disorder
focal
Refers to the more widespread involvement of glomerular injury (usually > 50% affected)
diffuse
used to describe the condition of hypercellularity of the glomeruli
proliferative
refers to the thickening of the glomeruli basement membrane
membranous
involves only the kidney and the cause of the disease is directly related to the kidney
primary glomerular disease
the injury is caused by a mechanism outside of the kidney which is what occurs with lupus or diabetes
secondary glomerular disease
There are three main patterns of injury seen in glomerular disorders -
- hypercellularity
- leukocytic infiltration
- formation of crescents
an increased number of cells in the glomerulus
hypercellularity
cellular proliferation of the mesangial or endothelial cells
hypercellularity
results from accumulation of cells made of proliferating epithelial cells and infiltrating leukocytes
formation of crescents
what tends to occur after an immune or inflammatory response
formation of crescents
results in a thickening of the capillary walls of the glomerulus
basement membrane thickening
what is the accumulation of homogeneous and eosinophilic cells in the lumen of the glomerular capillaries
hyalinosis
when extensive - it obliterates the glomerular capillary lumens
hyalinosis
usually occurs as a result of capillary wall injury and it is usually the end result of glomerular damage
hyalinosis
this is commonly seen with focal segmental glomerulosclerosis
hyalinosis
what is the accumulation of extracellular collagenous matrix
sclerosis
it may be limited to the mesangial cells or involve the capillary loops of the glomerulus or both
sclerosis
which is what happens with diabetic glomerulosclerosis
this may obliterate capillary lumens in the glomeruli and result in the formation of adhesions in the bowman’s capsule
sclerosis
is an abrupt reduction in renal function with oliguria
acute kidney injury
what is the mortality rate of AKI?
50-80%
What percent of hospitalized patients have AKI?
5%
it is usually reversible if the underlying cause is treated
AKI
There are 3 stages of AKI.
Describe stage 1
1 - creatinine 1.5-1.9 times higher than baseline or greater than or equal to 0.3mg/dL increase in creatinine
There are 3 stages of AKI. Describe stage 2
2 - a creatinine of 2-2.9 times higher than the baseline
There are 3 stages of AKI. Describe stage 3.
3 - creatinine of 3.0 times higher than the baseline or an
increase in serum creatinine to ≥ 4.0 mg/dL or the initiation of renal replacement
therapy or in person less than 18 years old a decrease in eGFR to < 35ml/minute
per 1.732
There are three categories of AKI and they include:
pre-renal, intra-renal or intrinsic, and
post-renal. These terms are very descriptive of the etiology and the pathophysiology of
AKI.
caused by impaired blood flow to the kidney resulting in a decreased
GFR.
Pre-renal AKI
Anything which decreases renal perfusion can cause a pre-renal AKI. Etiologies
include:
Vasoconstriction of renal arteries from medications or shock states.
• Hypotension
• Hypovolemia
• Hemorrhage
• Inadequate cardiac output i.e. heart failure
• NSAIDS
• Renal artery stenosis
is the most common cause of AKI.
Pre-renal AKI
Laboratory findings consistent with
AKI include
a FeNa of < 1% and a BUN:Creatinine ratio of > 20
A fractional excretion of sodium (FeNa) is used to
evaluate an acute kidney injury and to
differentiate between a pre-renal and acute tubular necrosis
It is a calculated measure
based off the serum sodium, serum creatinine, urine sodium and urine creatinine.
A fractional excretion of sodium (FeNa)
It is
reported as a percentage and is a marker of renal sodium excretion.
A fractional excretion of sodium (FeNa)
A FeNa which is less than 1% indicates
that the kidneys are conserving sodium and is
indicative of a pre-renal AKI.
A FeNA which is greater than 2% indicates
that the
kidneys are wasting sodium and is consistent with an acute tubular necrosis.
Values
between 1-2% are indeterminate and are not helpful in differentiating between the two
disease processes.
A fractional excretion of sodium (FeNa)
may be used to evaluate the etiology of an acute renal injury.
The BUN:Creatinine ratio
The ratio is a comparison between serum BUN and creatinine
The BUN:Creatinine ratio
It can be used to
differentiate between a pre-renal AKI or intra-renal AKI
The BUN:Creatinine ratio
A ratio that is greater than 20 is
consistent with a pre-renal acute kidney injury (AKI).
The BUN:Creatinine ratio
is caused by an issue which has impaired renal function at the cellular
level in the kidney
Intra-renal AKI
The two main causes of intra-renal AKI are:
Inflammatory conditions and acute tubular necrosis
What are some inflammatory conditions that cause intra-renal AKI
glomerulonephritis, vasculitis, drug induced
toxicity such as aminoglycosides
results in a severe necrosis of tubular epithelial cells.
The cells slough off and collect in the tubule and cause an obstruction
Acute Tubular necrosis (ATN)
This
obstruction causes an increase in tubular pressure that subsequently leads to a
decreased GFR.
acute tubular necrosis
The decrease in the GFR causes the afferent arteriole to vasoconstrict
and this decreases GFR even further. The increased tubular pressure also leads to back
flow of fluid into the renal interstitial tissue
acute tubular necrosis
What you will see clinically is a rising
creatinine and BUN. The creatinine will rise until it peaks. I have seen it go as high as
10 and then it will come down. When it starts coming down these individuals will
begin to diuresis and they can easily get dehydrated. Prior to this they are at risk for
volume overload. During the time the creatinine is rising, the individual is at risk for
electrolyte imbalances such as hyperkalemia, hyperphosphatemia, hypocalcemia etc.
Anytime the kidney is injured regardless of the cause, the person is at risk for
electrolyte and acid base imbalances that you see in CKD and potentially other
complications too.
acute tubular necrosis
Causes of ATN include
sepsis, post-surgical complications,
obstetrical complications, and medications
Any pre-renal etiology can be so profound
that it progresses to
ATN - acute tubular necrosis
ATN caused by ? is the most common cause of
intra-renal injuries.
ischemia
caused by a urinary tract obstruction such as bladder outlet obstruction.
Post-renal AKI
may occur as a result of prostatic hyperplasia or ureteral
obstruction from a urinary stone
A bladder outlet obstruction
An obstruction increases retrograde pressure and causes
an
ATN - acute tubular necrosis
Regardless of the origin of ARF, all forms of acute renal failure, if left
untreated, will all result in
ATN - acute tubular necrosis
Clinical manifestations of AKI are dependent upon the cause. Manifestations include:
• Oliguria, anuria
• Fatigue, edema, dyspnea
• Mental status changes secondary to uremia
• Electrolyte imbalances include hyperkalemia, hyponatremia.
• Metabolic acidosis
• BUN:Creatinine Ratio will be > 20 in a pre-renal AKI. It will be normal in intra-renal
AKI.
• FeNa will be < 1% in pre-renal AKI and > 2% in an ATN.
• Muddy Brown Cast cells are seen in the UA with ATN.
progressive and irreversible loss of nephron function.
CKD - chronic kidney disease
There are five stages of
CKD
The five stages are defined by the
GFR
CKD Stage I is defined by
a GFR of ≥ 90 ml/min.
a. These people are usually asymptomatic
• CKD Stage II is defined by
a GFR of 60-80 ml/min.
a. These individuals experience an increase in PTH, early bone disease,
increasing plasma creatinine and urea. They may have subtle hypertension.
• CKD Stage III is defined by
a GFR of 30-59 ml/min.
a. These individuals have erythropoietin deficiency, experience anemia, and have
an increase in creatinine and urea. They will have mild HTN.
CKD Stage IV is defined by
a GFR of 15-29 ml/min.
a. These individuals experience increased triglycerides, metabolic acidosis,
hyperkalemia, sodium and water retention and elevated BUN/creatinine.
Additional symptoms include moderate HTN, hyperphosphatemia, and anemia.
• CKD Stage V is defined by
a GFR of < 15 ml/min or the need for hemodialysis. This
results in uremia. They will also experience severe HTN, anemia and
hyperphosphatemia.
CKD usually occurs over a number of years as the internal structures of the kidneys are
slowly damaged by one or more of the following processes:
Diabetes is the most common cause.
• HTN is the second most common cause.
• Glomerulonephritis is the third most common cause.
• Polycystic kidney disease
• Obstructive problems such as renal stones
CKD begins with a chronic injury to the kidney which causes
an irreversible loss of
nephrons
The loss of nephrons causes an increase in
glomerular filtration pressure in
remaining nephrons. This increase in pressure causes hyperfiltration (HTN at the
nephron) of the remaining nephrons.
This causes more nephrons to fibrose and scar
resulting in
the loss of more nephrons. This will ultimately lead to uremia and the clinical
manifestations of CKD.
Eventually the individual will become oliguric and anuric. The
clinical manifestations include:
- Uremia
- Anemia
- Fluid and electrolyte imbalances
- secondary hyperparathyroidism
- decreased synthesis of vitamin D
- hypocalcemia
- Osteodystrophy
- normocytic anemia
- HTN
- altered mental status
- Insulin resistance
- CVD
- Impaired platelet function
is the accumulation of urea and other toxins which accumulate due to the
decrease in GFR and renal function.
Uremia
secondary to decrease erythropoietin levels. This can lead to left ventricular
hypertrophy.
Anemia
They include:
a. Hyperkalemia is common in late stages when the patient is oliguric. In early
stages potassium excretion is maintained.
b. Fluid volume deficit and Hyponatremia- during the early stages sodium and
fluid wasting occurs secondary to lack of the kidney’s ability to concentrate
urine.
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c. Fluid overload and hypernatremia occur in late stages as the patient becomes
oliguric. Sodium is not excreted and accumulates as does fluid.
d. Hyperphosphatemia occurs due to a decreased excretion of phosphorus.
e. Hypocalcemia occurs because calcium has an inverse relationship to
phosphorus. A decreased production of the active form of vitamin D
(calcitriol). This is needed for the absorption of calcium in the gut.
f. Metabolic Acidosis occurs because of the kidney’s inability to reabsorb urinary
bicarb (HCO3) or excrete H+
Fluid and electrolyte imbalances are common.
occurs to compensate for the low calcium levels
which are secondary to the hyperphosphatemia. Hyperphosphatemia occurs because
the kidneys are not able to excrete phosphorus. Most of phosphorus in the body comes
from the diet. Remember that phosphate binds with calcium and they have an inverse
relationship. When phosphorus is elevated, it binds more calcium which then
decreases the calcium level. This is the trigger for PTH secretion.
Secondary hyperparathyroidism
(calcitriol), therefore calcium absorption
is impaired.
Decreased synthesis of activated vitamin d
results from the secondary hyperparathyroidism. Remember PTH
causes an increase in osteoclastic activity, which causes the breakdown of bone.
Osteodystrophy is defective bone formation which leads to osteoporosis. The
metabolic acidosis associated with CKD also contributes to the development of
osteodystrophy.
Osteodystrophy
commonly occurs and is due to a decreased secretion of
erythropoietin from the kidney.
a normocytic anemia
occurs or worsens because failing kidneys secrete more renin. This results in
more angiotensin II and vasoconstriction.
HTN
can occur from the increased levels of urea and other uremic
toxins. This usually will not be seen unless the BUN is > 100.
Altered mental status
is common in CKD. Hyperparathyroidism decreases insulin
sensitivity and impairs glucose tolerance. As the kidney function decreases it is not
able to clear adiponectin and leptin which can contribute to the insulin resistance. Also
the failing kidney is not able to degrade insulin so insulin’s half life is prolonged.
Insulin resistance
is common in CKD. They tend to have high triglyceride levels, low
HDLs and high LDLs.
Dyslipidemia
is the main cause of death in persons with CKD. This is
secondary to the dyslipidemia that they experience, anemia, increase release or renin
and vascular calcification. All of these increase the risk for ischemic heart disease.
Cardiovascular disease
is caused by the uremic environment. Platelets are not able
to aggregate in a uremic environment.
Impaired platelet function
