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Renal failure Flashcards

1
Q

acute renal failure

A

-Sudden loss of kidney function resulting in:
-Lack of Acid-base maintenance
-Abnormal fluid and electrolyte management
-Loss of ability for excrete nitrogenous waste

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2
Q

acute renal failure: signs and symptoms

A

-Uremia:
-Nausea
-Vomiting
-Malaise
-Altered mentation*

-Perfusion defects:
-third spacing
-Edema
-Dizziness

-Electrolyte abnormality- Abdominal pain / ileus
-hypo/hyperkalemia -> ileus bc K influences muscle
-silent bowel

-Pericardial effusion- Pericardial Friction Rub
-Electrolyte abnormality- Arrhythmias

-Platelet dysfunction- Bleeding
-buildup of nitrogenous waste -> platelets dysfunction -> capillary bleeds

-Neurologic findings

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3
Q

acute renal failure: pre-renal

A

-BUN:creatinine ratio will be > 20:1 due to increased urea reabsorption
-Look at the cause of the failure for other findings
-why isnt blood getting to kidney?
-MC cause (40-80% of ARF cases)
-Due to renal hypo-perfusion:

-Volume depletion
-Dehydration
-GI loss
-Hemorrhage

-Vascular resistance
-Sepsis, anaphylaxis
-Afterload reducing medications (ACE-I and NSAIDS combo (dilation and constriction))* -> glomerulus affected
-Renal artery stenosis- CT angiography

-Low cardiac output
-post MI
-Heart failure, PE, pericardial tamponade
-Ventilator effect from positive end pressure ventilation
-make sure urine output starts up again after surgery

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4
Q

acute renal failure: renal (intrinsic) caused

A

-Accountable for 50% of cases

-Referral to:
-Nephrologist : if signs have been present for 1-2 weeks but no acute uremia -> physiological issue
-Urologist : if signs of urinary tract obstruction -> surgical/anatomical issue

-Admit to hospital when: Sudden loss of function with abnormalities that cannot be managed as an outpatient safely

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5
Q

acute renal failure: renal (intrinsic) caused -> dx and tx based on condition

A

-Acute Tubular Necrosis

-Interstitial Nephritis

-Glomerulonephritis

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6
Q

acute renal failure: post renal caused

A

-Least common cause (5-10%)
-elderly male
-urologist referral usually- surgical issue usually
-Typically easily reversed
-Caused by:
-Urethra obstruction
-Bladder dysfunction/obstruction
-Ureteral obstruction B/L (or unilateral if single kidney)
-BPH in men

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7
Q

catheters

A

-folley catheter-
-kuday catheter- stiffer to get past obstructions

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8
Q

acute renal failure: post renal caused -> findings and tx

A

-Anuria or frequent but small volume voids
-Suprapubic pain
-Palpably or percussed distended bladder or enlarged prostate
-High BUN/creatinine ratio (like pre-renal ARF)
-Ultrasound will often find the location of obstruction!!!

-Tx:
-Bladder catheterization to allow for release of urine
-Correction of underlying cause
-Followed by saliuresis (IV saline -> flush out kidneys) and diuresis

-Prompt treatment often leads to complete reverse of injury

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9
Q

acute renal failure: approach to testing

A

-When ARF is detected, the cause should always be determined so that treatment is focused accordingly

-Immediate diagnosis is critical, if you suspect:
-Decreased renal perfusion- Test for volume status and urine output
-Glomerulonephritis (intrinsic)- Test for urine sediment, serologic tests
-Urinary tract obstruction- Renal ultrasound will be diagnostic

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10
Q

diff dx of ARF

A

-can take a day
-casts

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11
Q

acute renal failure: clinical criteria for staging/prognosis**

A

-RIFLE/AKIN criteria

-Risk/Stage 1: 1.5 x increase in serum creatinine from the baseline OR <0.5 for 6-12hrs
-Injury/Stage 2: 2-3 x increase in serum creatinine from the pts baseline OR urine output <0.5 for > 12hr
-Failure/Stage 3- 3+x increase in serum creatinine from pts baseline OR decline of urine output to <0.3mL/kg/hr for 24 hr or anuria for 12 hours

-Correlated with Outcomes:
-Loss
-ESRD risk

-Acute Kidney Injury Network

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12
Q

acute renal failure: stage based management*******

A

-stage 1- why is there renal failure…work up pt
-stage 2- start decreasing meds, consider ICU (pts change status very fast)
-stage 3- renal replacement- dialysis

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13
Q

acute renal failure: contrast induced injury

A

-Changes in kidney function after administration of intravascular contrast media
-METFORMIN- BAD REACTION -> transition to sliding scale of insulin

-Prevent by prescreening for risk:
-History of prior kidney disease
-Fluid status: dehydration
-Diabetes: is the patient on metformin
-CHF/vascular disease: perfusion ability
-History of gout due to hyperuricemia
-Current use of nephrotoxic medications
-Recent exposure to IV contrast

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14
Q

acute renal failure: contrast induced injury- risk reduction

A

-NON-PHARMACOLOGIC
-Use lowest dose of IV contrast possible
-Assure adequate hydration prior to and following administration
-Decrease exposure to nephotoxic medications prior to and following

-PHARMACOLOGIC
-Consider IV volume expansion with isotonic saline or sodium bicarbonate in high risk patients has renal protective effect
-Oral n-acetylcysteine may be protective if given prior -> Be aware that allergic reaction may occur in up to 48% of people (not really used)
-Avoid use of diuretics

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15
Q

acute renal failure: tx with dialysis

A

-Initiate renal replacement therapy if: Life-threatening fluid, electrolyte or acid-base abnormalities exist
-Goals of treatment with dialysis are:
-Maintain homeostasis
-Prevent further injury to kidneys
-Permit renal recovery
-Allow treatment of underlying condition to proceed without complications

-Discontinue when patient is able to maintain by their own ability -> May need to attempt trial of intermittent dialysis (ween pt off) -> need to monitor closely

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16
Q

chronic kidney disease**

A

-a gradual, progressive loss of the ability to excrete wastes, concentrate urine, and conserve electrolytes
-memorize the stages

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17
Q

chronic renal failure

A

the continuing irreversible reduction in nephron number (corresponds to CKD Stages 3-5)

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18
Q

causes of CKD/CRF: pre/post/intra renal

A
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19
Q

pre-renal causes of CKD

A

-Caused by HYPOPERFUSION
-Examples:
-Renal artery stenosis-Fibromuscular Dysplasia

-Extrinsic Compression- tumor, anything compressing on artery

-Decreased Renal Perfusion Pressure- CHF

-Decreased Oncotic Pressure:
-Cirrhosis
-Nephrotic Syndromes (also intra-renal)

-fibromuscular dysplasia- females < 40

20
Q

intra-renal causes of CKD

A

-Intrinsic Renal Vascular Disease:
-Renal artery stenosis
-Glomerulosclerosis
-Recurrent thromboembolic disease
-hypoperfusion to kidney

-Glomerular Disease
-Nephritic/nephrotic syndromes

-Tubular and Interstitial Disease
-Nephrocalcinosis due to hypercalcemia or hypercalciuria
-Systemic Lupus Erythematosus
-Polycystic kidney disease (m/c genetic cause)
-Autoimmune

21
Q

post-renal causes of CKD

A

-Caused by Chronic OBSTRUCTION*

-Examples:
-Benign Prostatic Hyperplasia (BPH)
-Neoplasm

22
Q

summary of etiologies for chronic kidney disease

A

-pre-renal disease- CHF/cirrhosis
-post renal disease- BPH, obstructing malignancy
-intrinsic renal glomerular disease- nephritic/nephrotic

-intrinsic tubular and interstitial disease:
-Nephrocalcinosis due to hypercalcemia or hypercalciuria
-Systemic Lupus Erythematosus
-Polycystic kidney disease (m/c genetic cause)
-Autoimmune- Sjögren’s Syndrome and Sarcoidosis

-intrinsic renal vascular disease:
-Renal artery stenosis
-Glomerulosclerosis
-Recurrent thromboembolic disease- from previous renal artery dissection or aneurism

-MC CAUSES* :
-Diabetic glomerular disease
-Hypertensive nephropathy- primary glomerulopathy w/ HTN and vascular and ischemic renal disease
-Chronic glomerulonephritis

23
Q

pathophysiology: mechanisms of damage

A

-Initiating -> Initial loss of nephron mass
-Immune complexes
-Hypertension/Diabetes

-Progressive -> Maladaptive compensatory changes:
-Activation of Renin-Angiotensin-Aldosterone-System (RAAS)
-Hyperfiltration! of remaining viable nephrons
-Release of vasoactive hormones, cytokines, growth factors
-Maladaptative hypertrophy! and sclerosis
-Further reduction in renal mass
-unfunctional flow

24
Q

sodium and water homeostasis

A

-Extra-Cellular Fluid Volume (ECFV) Expansion - Dietary sodium intake > Urinary sodium excretion -> tendency for fluid overload
-decrease GFR -> increase salt/water retention -> increase vascular volume (fluid overload) -> increase hydrostatic pressure -> edema
-increase salt water retention can also lead to HTN and then HF
-increase vascular volume (fluid overload) can lead to HF

-tx-
-Dietary Salt/fluid restriction +/- diuretics (usually loops) -> if HF and edema
-Dialysis if non-responsive to diuretics

-ECFV Depletion
-Extra-renal salt/fluid loss -> impaired salt/water reabsorption -> ECFV depletion
-Common cause of “Acute-on-chronic Renal Failure”

-Excess free water consumption- Free water consumption > Urinary free water excretion -> hyponatremia

25
potassium homeostasis (common issue in CKD)
-decrease GFR -> decreased ability to excrete K -> hyperkalemia -exacerbation of hyperkalemia: -increased intake -transcellular shift -decreased excretion -effect of hyperkalemia: -impaired neuromuscular transmission: -muscle weakness -life threatening arrythmias -which ECG finding? -malaise -during hyperkalemia- gut starts taking on more excretion -management: -limit dietary K -avoidance of meds that cause hyperkalemia -dialysis in presence of ECG changes
26
metabolic acidosis (issue in severe CKD- stage 4/5)
-CKD -> H+ retention -effects: -chronic metabolic acidosis - big belly, skinny limbs -osteoporosis- via slow release of Ca hydroxyapatite from bone matrix -protein catabolism -muscle wasting -tx- sodium bicarbonate PO daily
27
hematologic effects of CKD: anemia*
-normocytic, normochromic -Primary Cause: Erythropoietin (EPO) deficiency -Other causes: -Iron Deficiency -Anemia of Chronic Disease (impaired iron utilization) -Bone marrow fibrosis -Treatment: -Recombinant EPO (darbopoetin-alpha) -decreases risk associated with repeat blood transfusions
28
hematologic effects of CKD- impaired platelet function*
-Primary Cause: UREMIA -Decreased activity of platelet factor III -Abnormal aggregation and adhesiveness -Prolonged bleeding time
29
hematologic effects of CKD: impaired immune function*
-Primary Cause- UREMIA -impaired WBC function -Leukocyte suppression/impaired degranulation -Other factors: acidosis/malnutrition
30
normal calcium/phosphate homeostasis
-vitamin D -> 25-OH vit D -> 1-25-(OH)2 vit D -> calcium absorption from the gut -> maintenance of Ca2+ homeostasis -slide 35, 36? -chronic kidney disease- 25 OH vit D NORMAL (made in liver) -1-25 (OH)2 Vit D -> ABNORMAL -> KIDNEY does not converts to active form in disease -phosphate retention -> hypocalcemia -hypocalemia -causes increase PTH -> bone manifestations, uremic manifestations -bones look cancerous but its not (brown tumors)
31
bone manifestation of CKD/renal osteodystrophy
-hypocalcemia: -impaired osteoid mineralization by osteoblasts -osteomalacia- accumulation of unmineralized bone matrix -hyperparathyroidism- increased osteoclast activity/calcium resorption from bone -osteitis fibrosa cystica: -abnormal osteoid -bone marrow fibrosis -formation of cysts- +/- hemorrhage, brown tumors -osteomalacia + osteitis fibrosa cystica +/- osteoporosis = renal osteodystrophy -(barely touched on this)
32
causes of hypocalcemia
-Malabsorption -Vitamin D deficiency -Chronic kidney disease -Loop diuretic use -Hypoparathyroidism -Pancreatitis -Septic shock -Hyperphosphatemia -(barely touched on this)
33
causes of hypercalcemia
-Milk-alkali syndrome -Vitamin D toxicity -Hyperparathyroidism -Pheochromocytoma -Thyrotoxicosis -PTH producing tumor -Multiple myeloma -Lymphoma -Thiazide diuretic use -Lithium use -(barely touched on this)
34
chronic kidney disease: management goals
-Slow and delay progression to complete renal failure (stage 5) -Treat associated symptoms of renal failure -Avoid damage to other organ systems -Limit disability -usually dont get better but you can stop progression
35
chronic kidney disease: primary prevention
-Encourage healthy lifestyles in patients -Diet -Exercise -Avoidance of substance abuse -Identifying patients at higher initial risk
36
chronic kidney disease: secondary prevention
-After risk factors begin- Such as DM or HTN -Initiate aggressive treatment -Targeted drug regiments know to prevent progression to renal disease -ACE-Inhibitors in DM -> any microalbumin in urine -> put them on -Initiate aggressive screening for renal involvement
37
chronic kidney disease: tertiary prevention/treatment
-Diagnosis of chronic renal impairment -Focus shifts from prevention of disease to treating disease and/or associated effects -Planning for future complications begins
38
delaying progression of renal disease
-Aggressive treatment of underlying cause -HTN -Aggressive BP management with goals of SBP < 120 and DBP < 80 -usually requires multiple medications -Dyslipidemia -LDL goal of 100 (unless indicated for lower) -Aggressive treatment of triglycerides -DM -Aggressive glycemic control with HbA1c goal of <7% -*Oral hypoglycemics need to be used with caution in advanced CKD -Metformin may lead to lactic acidosis -Thiazolidinediones lead to increased cardiac events -ACE-Inhibitors are encouraged for diabetics with proteinuria * -Recent studies have not shown clear renal benefits in very early stages -Monitor Potassium level -Avoid ACE-I in advanced CRF (stage 4-5) * -Avoid with Renal Artery Stenosis -Avoid medications/treatments that may further damage kidney function -Commonly used medications/treatments that cause renal dysfunction include: -IV contrast for CT -NSAIDs -Aminoglycosides
39
management of chronic kidney disease
-renal replacement therapy: -preparation of kidney replacement -> stage 4- GFR 15-29 -kidney replacement tx -> stage 5- GFR < 15 -pts should be educated to ds progression and anticipatory care throughout care -dialysis: -hemodialysis -peritoneal dialysis -renal transplantation: -best potential for complete recovery -typically dialysis tx is needed prior to transplant option
40
chronic renal disease morbidity/mortality
-Hospitalization and increased morbidity: -Dialysis patients average 2 hospital admissions/yr -Patients s/p renal transplant average 1 admission/yr -5 year survival ESRD = 35% -Coupled with DM = 25% -Transplantation increases the survival of patients with stage 5 CKD significantly -MC cause of death in CKD patients is Cardiovascular Disease****** -MC cause of chronic kidney disease -> DM!!!
41
dialysis
-HEMODIALYSIS -MC form of renal replacement in the US -Requires vascular access -Complications: -Hypotension is most common -Muscle cramping and anaphylatoid reactions can occur -PERITONEAL DIALYSIS -Infusion of a dextrose containing solution into the peritoneal cavity and then allowed to dwell for a period of time -Access by peritoneal catheter -Complications: -Peritonitis -Metabolic complications
42
hemodialysis
-MC form of renal replacement -Move solutes across a semi-permeable membrane by: -Diffusive clearance -Ultra-filtration -Solvent drag -access: -*AV fistula – preferred access form -AV graft -Venous catheter(least preferred)
43
renal transplant
-Start planning for transplant options when planning for renal replacement with dialysis -Donor Selection -Live- Typically family relative with matched HLA -Deceased- Testing to ensure HIV/Hepatitis negative serology -Malignancy/failure risk
44
MC opportunistic infection in renal transplant
-Peritransplant (<1 month) -Wound infections -Herpesvirus -Oral candidiasis -Urinary tract infection -Early (1–6 months) -Pneumocystis carinii -Cytomegalovirus -Legionella -Listeria -Hepatitis B -Hepatitis C -Late (>6 months) -Aspergillus -Nocardia -BK virus (polyoma) -Herpes zoster -Hepatitis B -Hepatitis C
45
post transplant complications
-Malignancy- 5-6% of patient on immunosuppressive therapy will develop cancer -Hypercalcemia -Hypertension -Hepatitis -Immunosuppressive therapy decreases immune control of Hepatitis B and C (test prior to transplant to counsel)
46
outcomes following renal transplant
-Improved quality of life and decreased disability when compared to dialysis -Improved life expectancy Compare to 5 year survival rate of 34% in dialysis population -Highest mortality post transplant is in the 1st year

Nephrology (8 decks)

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