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Renal Part I Flashcards

1
Q

What are the functions of the kidney?

A

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

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2
Q

Acidosis

A

pH is <7.38
Life is threatened when <7.25
Death occurs if <7

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3
Q

Alkalosis

A

pH is >7.42
Very dangerous when pH is >7.55
Death occurs when pH is >7.6

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4
Q

Regulation of pH

A

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)

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5
Q

Waste removal

A

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

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6
Q

Waste removal: glomerular capsule

A

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)

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7
Q

Causes of vit D deficiency

A 
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
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8
Q

Vit D deficiency consequences

A 
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
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9
Q

Excretion

A

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

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10
Q

Renal corpuscle

A

Production of filtrate

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11
Q

Proximal convoluted tubule

A

Reabsorption of water, ions, and all organic nutrients

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12
Q

Loop of Henle

A

Further reabsorption of water (descending limb) and both sodium and chloride ions (ascending limb)

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13
Q

Distal convoluted tubule

A

Secretion of ions, acids, drugs, toxins

Variable reabsorption of water, sodium ions, and calcium ions (under hormonal control)

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14
Q

Collecting duct

A

Variable reabsorption of water and reabsorption or secretion of sodium, potassium, hydrogen, and bicarb ions

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15
Q

Papillary duct

A

Delivery of urine to minor calyx

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16
Q

BUN

A

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

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17
Q

Things that elevate BUN

A 
Urinary tract obstruction
CHF or recent MI
Severe GI bleeding
Dehydration/hypovolemia
High protein diet
Certain meds, esp abx
RENAL FAILURE
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18
Q

Things that may decrease BUN

A

Severe liver dz
Anabolic state (starvation)
SIADH

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19
Q

Creatinine

A

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

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20
Q

Causes of elevation in creatinine

A 
Dehydration
Dietary supplements
Large meat intake
Meds
-Cimetidine
-Trimethoprim
-Ranitidine
-Ceaphalosporins
-Fenofibrate
Medical conditions
-DKA
-Pyelonephritis
-Urinary tract obstruction
-Rhabdomyolysis
KIDNEY FAILURE
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21
Q

Causes of decrease of creatinine

A

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)

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22
Q

Clearance

A

Rate at which a substance is removed from plasma

How much blood the kidneys can make creatinine free in one min

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23
Q

What is CrCl used to estimate?

A

GFR

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24
Q

GFR

A

Measures how well kidneys are filtering blood

Reduced GFR= retention of nitrogenous waste

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25
There is a ______ relationship between clearance and serum creatinine
Inverse
26
FENA
Fractional excretion of Na | Used to help differentiate pre-renal vs extra-renal process
27
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
28
What does an FENA > 1 % indicate?
ATN | Failing kidney, cannot compensate, leaks sodium, indicates kidney dx
29
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
30
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) ```
31
Risk and GFR criteria
Increased creatinine x 1.5 or GFR decrease >25%
32
Risk and urine output criteria
UO < 0.5 mL kg-1h-1 x 6h
33
Injury and GFR criteria
Increased creatinine x2 or GFR decrease >50%
34
Injury and urine output criteria
UO <0.5 mL kg-1h-1 x 12h
35
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)
36
Failure and urine output criteria
UO <0.3 mL kg-1h-1 x 24h or anuria x 12h
37
Loss criteria
Persistent ARF = complete loss of renal function >4 wks
38
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 ```
39
S/sx of AKI
``` Nausea and vomiting Malaise AMS HTN Asterixis ```
40
Anuria
No urine output OR <100 cc/24 hrs OR <0.5 cc/kg/hr
41
Oliguria
<500 cc/24 hrs OR <20 cc/hr OR <1cc/kg/hr
42
Polyuria
>2.5L/24 hrs
43
Prerenal AKI
Sudden and severe drop in BP (shock) or interruption of blood flow to the kidneys from severe injury or illness
44
Intrarenal AKI
Direct damage to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply
45
Postrenal AKI
Sudden obstruction of the urine flow due to enlarged prostate, kidney stones, bladder tumor, or injury
46
Causes of prerenal AKI
``` MCC of acute kidney injury Hypovolemia -Hemorrhage Dehydration Increased GI losses 3rd space losses Hypoxia Sepsis Cardiac failure Hypotention ```
47
Causes of postrenal AKI
``` Obstruction Stones BPH Tumor Trauma Spinal cord lesion ```
48
Dx of postrenal AKI
US (hydronephrosis) | CT if you suspect stones
49
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 ```
50
Drugs that can cause intrarenal AKI
``` ACE inhibitors ARBs NSAIDs Tramadol Toradol IV contrast dye Amphotericin B Aminoglycosides IV acyclovir ```
51
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)
52
What are the three major classifications of intrarenal AKI
ATN Acute glomerulonephritis Acute interstitial nephritis
53
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)
54
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 ```
55
Phases of ATN
Initiating phase Maintenance phase Recovery phase
56
Initiating phase of ATN
Lasts ~24-36 hrs from time of injury | Progressive azotemia, progressive oliguria
57
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 ```
58
Recovery phase of ATN
Polyuria Hypokalemia Decreasing azotemia Pts tend to need fluid resuscitation and close monitoring of electrolytes
59
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
60
Generalized tx of ATN
``` Refer to nephrologist Avoid volume overload Avoid hyperkalemia Dietary protein restriction Treat electrolyte imbalances carefully Dialysis if needed ```
61
Indications for dialysis
``` Acid/base disorders Electrolyte imbalances Intoxication Overload of volume Uremia ```
62
Acute interstitial nephritis
Immune-mediated cause of acute renal failure | Typically secondary to an allergic reaction, drug reaction, infection, or granulomatous dz
63
Common presentation of acute interstitial nephritis
50-60s female with fever, arthralgia, rash, and hematuria
64
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
65
What infections can AIN follow?
``` Pyelonephritis Staph Strep CMV EBV Hep C Mycoplasma Rocky Mountain Spotted Fever ```
66
When can granulomatous interstitial nephritis be seen?
Sarcoidosis SLE Sjogrens Renal tuberculosis
67
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 ```
68
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
69
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
70
Tx of AIN
Recovery takes weeks to months Supportive measures Remove inciting agent Short-term, high-dose prednisone IV with taper
71
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 ```
72
Nephrotic syndrome
Hypoalbuminemia Hyperlipidemia Peripheral edema Massive proteinuria
73
Urine casts in nephrotic syndrome
Fatty casts
74
Urine casts in nephritic syndrome
RBC casts; | Cola/smoky urine
75
Proteinuria in nephrotic syndrome
> 3.5 g/day
76
Proteinuria in nephritic syndrome
< 3.5 g/day
77
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 ```
78
What do most patients with nephrotic syndrome also have?
``` DM Amyloidosis SLE Other causes: Minimal change dz Membranous nephropathy Idiopathic ```
79
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
80
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
81
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
82
Glomerulonephritis
Antigen-antibody complex in glomeruli causing: - Inflammation - Decreased GFR
83
S/sx of glomerulonephritis
``` HA Increased BP Facial/periorbital edema Lethargic Low-grade fever Weight gain (edema) Proteinuria Hematuria Oliguria Dysuria ```
84
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
85
Labs for glomerulonephritis
``` +ASO titer + complement anti-GBM ANCA ANA Cryoglobin panel Hep panel U/A: hematuria, proteinuria, RBCs, WBCs, RBC casts = pathognomonic ```
86
Diagnostics for glomerulonephritis
Renal u/s | Biopsy
87
Tx for glomerulonephritis
Supportive High-dose steroids -60 mg/day x 12 wks
88
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 ```
89
S/sx of acute glomerulonephritis
Hypertension Edema most commonly in low tension tissue areas like the scrotum and periorbital area Hematuria
90
Lab results for acute glomerulonephritis
``` BUN:Cr >20:1 Urine Na <20 FENA <1 Low serum albumin May have hyperlipidemia ```
91
Tx for acute glomerulonephritis
Depends on the cause, high-dose steroids are sometimes used
92
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
93
Presentation of Berger disease
Gross hematuria with upper respiratory tract infection | Occurs 1-2 days after initial URI sx or "synpharyngitic hematuria"
94
Dx of Berger dz
Renal bx: IgA and C3 deposits
95
Tx of Berger dz
Depends on the extent of the dz HTN prevention Renal transplant in some cases
96
Post-infectious glomerulonephritis
Seen most commonly following a GABHS infection and occurring on average 7-10 days after initial infection
97
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
98
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
99
Generalized sx of Goodpasture syndrome
``` Anorexia Fatigue Fever Arthralgia Weakness ```
100
Lung sx of Goodpasture syndrome
Hemoptysis Dry cough CP SOB
101
Renal sx of Goodpasture syndrome
Hematuria RBC casts Low level proteinuria
102
CXR on Goodpasture syndrome
Fluffy infiltrates up to massive pulmonary hemorrhage
103
Dx of Goodpasture syndrome
Confirmed by finding anti-GBM antibodies

CAM III (12 decks)

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