Renal Part I Flashcards
What are the functions of the kidney?
Regulation of extracellular fluid volume and BP
-Renin synthesis (increases BP and blood volume)
Regulation of osmolarity and iron balance
Homeostatic regulation of pH
Erythropoietin synthesis
-Releases retics from bone marrow
Vit D synthesis (active form)
-Regulates mineral homeostasis
Gluconeogenesis in times of starvation
Waste removal
Acidosis
pH is <7.38
Life is threatened when <7.25
Death occurs if <7
Alkalosis
pH is >7.42
Very dangerous when pH is >7.55
Death occurs when pH is >7.6
Regulation of pH
The pH of urine may vary from as low as 4.5 to as high as 9.8 depending on what condition the kidney is trying to overcome
Kidneys can:
-Excrete H+ ions
-Reabsorb bicarb
-Excrete titratable acid (net acid excretion)
-Excrete NH4+ (ammonium)
Waste removal
Afferent arterioles bring blood from the renal artery (dirty blood) into the glomerulus of the nephron
Efferent arterioles carry filtered blood away from the glomerulus
Afferent arterioles are larger, causing a pressure buildup within the glomerulus which facilitates waste removal
Waste removal: glomerular capsule
The glomerular capillary wall determines what is filtered and how much is filtered
It has three layers:
-Endothelium: allows plasma proteins and fluid through, but not RBCs
-Basement membrane: prevents plasma proteins exiting the bloodstream
-Epithelium: filtration level of fluid within the glomerular space (podocytes)
Causes of vit D deficiency
Sun: -Sunscreen -Melanin -Latitude -Winter Meds and supplements -Antiseizure meds -Glucocorticoids -Rifampin -HAART -St. John's wart Hepatic failure Renal failure Nephrotic syndrome Obesity Malabsorption -Crohn's -Whipple -CF -Celiac -Liver dz
Vit D deficiency consequences
Schizophrenia Depression Infections -URI -TB Decreased FEV1 Asthma and wheezing diseases HBP CHD AODM Syndrome X Autoimmune diseases -Type 1 DM -MS -Crohn's -RA Cancer -Breast -Colon -Prostate -Pancreas Muscle weakness Muscle aches Osteoarthritis Osteomalacia Rickets
Excretion
The nephron is the basic structural and functional unit of the kidney which allows for filtration
Fluid passes through the tubules and is modified either by reabsorption or secretion
Reabsorption removes substances from the filtrate back into the system
Secretion adds substances to the filtrate for excretion
Fluid enters Bowman’s space then into the loop of Henle. The bulk of the filtered solute and water are resorbed
The collecting tubules make the final urinary composition changes and allow solute and water excretion to vary with alteration in dietary intake
Renal corpuscle
Production of filtrate
Proximal convoluted tubule
Reabsorption of water, ions, and all organic nutrients
Loop of Henle
Further reabsorption of water (descending limb) and both sodium and chloride ions (ascending limb)
Distal convoluted tubule
Secretion of ions, acids, drugs, toxins
Variable reabsorption of water, sodium ions, and calcium ions (under hormonal control)
Collecting duct
Variable reabsorption of water and reabsorption or secretion of sodium, potassium, hydrogen, and bicarb ions
Papillary duct
Delivery of urine to minor calyx
BUN
Nl range 3-20 mg/dL
Urea is produced as a byproduct of metabolism in the liver which is then released into the blood to be removed in the urine
A measure of renal function (and liver function)
High BUN levels generally indicate poor renal function
Things that elevate BUN
Urinary tract obstruction CHF or recent MI Severe GI bleeding Dehydration/hypovolemia High protein diet Certain meds, esp abx RENAL FAILURE
Things that may decrease BUN
Severe liver dz
Anabolic state (starvation)
SIADH
Creatinine
Chemical by-product of muscle function
Nl range: 0.6-1.2 mg/dL
Produced by creatine
About 2% of body’s creatine is converted to ccreatinine daily
Transported through the blood to the kidneys, whose job is to filter out and dispose most of it
Muscle mass doesn’t change daily, so creatinine shouldn’t either
Causes of elevation in creatinine
Dehydration Dietary supplements Large meat intake Meds -Cimetidine -Trimethoprim -Ranitidine -Ceaphalosporins -Fenofibrate Medical conditions -DKA -Pyelonephritis -Urinary tract obstruction -Rhabdomyolysis KIDNEY FAILURE
Causes of decrease of creatinine
Generally less worrisome than increase
Decreased muscle mass (aging, dz)
Ultra low protein diet (not uncommon in vegans)
Pregnancy
Cachexia (severe malnutrition, cancer)
Severe liver dz (interferes with creatinine production)
Clearance
Rate at which a substance is removed from plasma
How much blood the kidneys can make creatinine free in one min
What is CrCl used to estimate?
GFR
GFR
Measures how well kidneys are filtering blood
Reduced GFR= retention of nitrogenous waste
There is a ______ relationship between clearance and serum creatinine
Inverse
FENA
Fractional excretion of Na
Used to help differentiate pre-renal vs extra-renal process
What does an FENA <1% indicate?
Prerenal cause, volume depletion
Kidney corrects for low fluid state by reabsorbing Na, indicates functional kidney
Hypovolemia, CHF, RAS, sepsis, contrast-induced nephropathy will often look pre-renal
What does an FENA > 1 % indicate?
ATN
Failing kidney, cannot compensate, leaks sodium, indicates kidney dx
Acute kidney injury
Refers to sudden loss or deterioration of kidney function resulting in an inability to maintain acid-based, fluid and electrolyte balance and to excrete nitrogenous wastes
RIFLE criteria
The most commonly used criteria for determining the severity and extent of renal failure Risk Injury Failure Loss (of function) End stage renal dz (ESRD)
Risk and GFR criteria
Increased creatinine x 1.5 or GFR decrease >25%
Risk and urine output criteria
UO < 0.5 mL kg-1h-1 x 6h
Injury and GFR criteria
Increased creatinine x2 or GFR decrease >50%
Injury and urine output criteria
UO <0.5 mL kg-1h-1 x 12h
Failure and GFR criteria
Increased creatinine x3 or GFR decrease >75% or creatinine >4 mg per 100 mL (acute rise of >0.5 mg per 100 mL)
Failure and urine output criteria
UO <0.3 mL kg-1h-1 x 24h or anuria x 12h
Loss criteria
Persistent ARF = complete loss of renal function >4 wks
AKI- components
Sudden, hours or days, may be reversible Often iatrogenic Can be pre/intra/post renal cause Identify the cause and treat More common in pts with some CKD already present
S/sx of AKI
Nausea and vomiting Malaise AMS HTN Asterixis
Anuria
No urine output OR
<100 cc/24 hrs OR
<0.5 cc/kg/hr
Oliguria
<500 cc/24 hrs OR
<20 cc/hr OR
<1cc/kg/hr
Polyuria
> 2.5L/24 hrs
Prerenal AKI
Sudden and severe drop in BP (shock) or interruption of blood flow to the kidneys from severe injury or illness
Intrarenal AKI
Direct damage to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply
Postrenal AKI
Sudden obstruction of the urine flow due to enlarged prostate, kidney stones, bladder tumor, or injury
Causes of prerenal AKI
MCC of acute kidney injury Hypovolemia -Hemorrhage Dehydration Increased GI losses 3rd space losses Hypoxia Sepsis Cardiac failure Hypotention
Causes of postrenal AKI
Obstruction Stones BPH Tumor Trauma Spinal cord lesion
Dx of postrenal AKI
US (hydronephrosis)
CT if you suspect stones
Causes of intrarenal AKI
Direct damage to the kidney Acute tubular necrosis (MC) Inflammation -Acute interstitial nephritis Toxins (heavy metals, solvents) Drugs Infection (glomerulonephritis, pyelonephritis) Blood supply
Drugs that can cause intrarenal AKI
ACE inhibitors ARBs NSAIDs Tramadol Toradol IV contrast dye Amphotericin B Aminoglycosides IV acyclovir
How to prevent ATN from contrast dye
N-acetylcysteine (Mucomyst)- used by RTs in nebs and given orally for acetaminophen overdose can also be used as a preventative medication before administering IV contrast dye to lower the likelihood of developing ATN
Dosed as 600 mg orally every 12 hrs, once before and once after a dye load (or occasionally 1200 mg IV once before emergent surgery or contrast administration)
What are the three major classifications of intrarenal AKI
ATN
Acute glomerulonephritis
Acute interstitial nephritis
Causes of ATN
85% of intrarenal dz
Typically results from necrosis secondary to extended hypovolemia (surgery, burns, hemorrhage)
OR nephrotoxic meds or both
Endogenous cause: myoglobin (rhabdo)
Lab results in ATN
BUN:Cr is >20:1 Hyperkalemia, hyperphosphatemia Urine Na >40 mEq/L Spec gravity <1.010 Fractional excretion of Na >1% Urine osmolality typically around 350 UA will show granular (muddy brown) casts, renal tubular casts
Phases of ATN
Initiating phase
Maintenance phase
Recovery phase
Initiating phase of ATN
Lasts ~24-36 hrs from time of injury
Progressive azotemia, progressive oliguria
Maintenance phase of ATN
Oliguria (40-400 mL/24 hrs) High azotemia Metabolic acidosis Hyperkalemia; may be highly transient and not evident clinically 50% of the time Period of 1-2 weeks Pts may require dialysis
Recovery phase of ATN
Polyuria
Hypokalemia
Decreasing azotemia
Pts tend to need fluid resuscitation and close monitoring of electrolytes
Tx of ATN
Primary goal: prevent further injury
If they are fluid deficient or hypotensive, address with IVF and inotropes
Treat any underlying sepsis
D/C all nephrotoxic drugs
-And adjust dosage on all renally excreted meds
If BP and cardiac stable may use loop diuretics to deal with oliguria
Good evidence supports dialysis before complications arise
Generalized tx of ATN
Refer to nephrologist Avoid volume overload Avoid hyperkalemia Dietary protein restriction Treat electrolyte imbalances carefully Dialysis if needed
Indications for dialysis
Acid/base disorders Electrolyte imbalances Intoxication Overload of volume Uremia
Acute interstitial nephritis
Immune-mediated cause of acute renal failure
Typically secondary to an allergic reaction, drug reaction, infection, or granulomatous dz
Common presentation of acute interstitial nephritis
50-60s female with fever, arthralgia, rash, and hematuria
Medication-induced acute interstitial nephritis
70% of AIN cases
Occurs around 2 wks after new med
Commonly abx: PCN, cephalosporin, bactrim
If induced by NSAIDs is associated with nephrotic syndrome
What infections can AIN follow?
Pyelonephritis Staph Strep CMV EBV Hep C Mycoplasma Rocky Mountain Spotted Fever
When can granulomatous interstitial nephritis be seen?
Sarcoidosis
SLE
Sjogrens
Renal tuberculosis
PE of AIN
General malaise Nausea (from buildup of metabolites) Polydypsia and polyuria (kidneys unable to concentrate urine appropriately) Nl BP: NO edema (distinguishes from ATN) -Unless from NSAIDs If drug induced: maculopapular rash
Lab results of AIN
Progressive increase in BUN and creatinine
UA will show WBCs, white cell casts
-Sterile pyuria (WBCs but no infection- eosinophils)
-90% also have hematuria
-Proteinuria if NSAID induced
CBC: eosinophilia in 80% of cases
Dx of AIN
Gold standard is renal bx
Not needed in all pts (if you can be confident of dx without it)
Pts who do NOT improve after withdrawal of supposed offending agent WOULD benefit
Pts refusing bx can have renal u/s, but not as specific
Tx of AIN
Recovery takes weeks to months
Supportive measures
Remove inciting agent
Short-term, high-dose prednisone IV with taper
Nephritic syndrome
Inflammation of the glomeruli Oliguria HTN Cola-colored urine (hematuria) Berger's dz (IgA nephropathy) is the most common cause of primary glomerulonephritis
Nephrotic syndrome
Hypoalbuminemia
Hyperlipidemia
Peripheral edema
Massive proteinuria
Urine casts in nephrotic syndrome
Fatty casts
Urine casts in nephritic syndrome
RBC casts;
Cola/smoky urine
Proteinuria in nephrotic syndrome
> 3.5 g/day
Proteinuria in nephritic syndrome
< 3.5 g/day
Nephrotic disease
Bland urine sediment Urine protein exceeds 3g per 24 hrs Hypoalbuminemia (albumin <3 g/dL) Peripheral edema Hyperlipidemia Elevated ESR Hypercoagulability Oval fat bodies in the urine Renal bx may be helpful
What do most patients with nephrotic syndrome also have?
DM Amyloidosis SLE Other causes: Minimal change dz Membranous nephropathy Idiopathic
Tx of nephrotic syndrome
Avoid negative nitrogen balance, replace protein last in urine
Low sodium diet, diuretics
Treat hyperlipidemia, hypercoagulable state
-Loss of protein C, protein S, antithrombin III
-Danger of renal vein thrombosis
Minimal change dz
MCC of proteinuric renal dz in children, accounting for 80% of cases
S/sx of nephrotic syndrome: proteinuria, hypoalbuminemia, facial edema
In adults, there is a correlation with Hodgkin’s dz
Glomeruli show no changes on light microscopy. On electron microscopy, there is a characteristic effacement of the podocyte foot process
Multiple myeloma/amyloid
Cancer of the plasma cells
Accumulation of protein in various organs
-Part of a series of protein-deposition diseases
Proteinuria, hypercalcemia
u/s- normal size kidneys
Dx- kidney or bone bx
Tx- oncology management with dialysis at end stage
Glomerulonephritis
Antigen-antibody complex in glomeruli causing:
- Inflammation
- Decreased GFR
S/sx of glomerulonephritis
HA Increased BP Facial/periorbital edema Lethargic Low-grade fever Weight gain (edema) Proteinuria Hematuria Oliguria Dysuria
Demographics of glomerulonephritis
Usually children, ages 2-12 yrs
Status post group A strep infection= within 1-3 wks
-Can occur even after appropriate strep infection tx
RBC casts, hematuria, HTN
Labs for glomerulonephritis
\+ASO titer \+ complement anti-GBM ANCA ANA Cryoglobin panel Hep panel U/A: hematuria, proteinuria, RBCs, WBCs, RBC casts = pathognomonic
Diagnostics for glomerulonephritis
Renal u/s
Biopsy
Tx for glomerulonephritis
Supportive
High-dose steroids
-60 mg/day x 12 wks
Acute glomerulonephritis in adults
Relatively uncommon UA: RBC casts Several types, including: -Berger dz: MC in adults -Peri-infection or post-infection glomerulonephritis - Lupus nephritis -Goodpasture syndrome (anti-GBM-associated acute glomerulonephritis) -Pauci- immune glomerulonephritis --Seen in vasculitis pts
S/sx of acute glomerulonephritis
Hypertension
Edema most commonly in low tension tissue areas like the scrotum and periorbital area
Hematuria
Lab results for acute glomerulonephritis
BUN:Cr >20:1 Urine Na <20 FENA <1 Low serum albumin May have hyperlipidemia
Tx for acute glomerulonephritis
Depends on the cause, high-dose steroids are sometimes used
Berger disease
Cause: IgA deposition in the glomerular mesangium
Can also occur as a secondary dz associated with hepatic cirrhosis, celiac dz, HIV, CMV, GABHS
M > F
Children > adults
Tends to present in individuals of Asian descent
Presentation of Berger disease
Gross hematuria with upper respiratory tract infection
Occurs 1-2 days after initial URI sx or “synpharyngitic hematuria”
Dx of Berger dz
Renal bx: IgA and C3 deposits
Tx of Berger dz
Depends on the extent of the dz
HTN prevention
Renal transplant in some cases
Post-infectious glomerulonephritis
Seen most commonly following a GABHS infection and occurring on average 7-10 days after initial infection
Presentation of post-infectious glomerulonephritis
Appears most frequently in children and presents with abrupt onset of nephritic sx and acute kidney injury
Rising ASO titers and low complement levels can be seen
Goodpasture syndrome
The clinical constellation of glomerulonephritis and pulmonary hemorrhage
Bimodal distribution in the second/third decades of life and again in the sixth/seventh decades
Generalized sx of Goodpasture syndrome
Anorexia Fatigue Fever Arthralgia Weakness
Lung sx of Goodpasture syndrome
Hemoptysis
Dry cough
CP
SOB
Renal sx of Goodpasture syndrome
Hematuria
RBC casts
Low level proteinuria
CXR on Goodpasture syndrome
Fluffy infiltrates up to massive pulmonary hemorrhage
Dx of Goodpasture syndrome
Confirmed by finding anti-GBM antibodies
