Renal Part II Flashcards
Sx of associated with hematuria
Colic
Frequency/burning
Intermittent
Med hx associated with hematuria
Anticoagulants
Analgesics
Sickle cell
Abx
Work up for hematuria
U/A with microscopy= casts often make the dx -Red cell cast= glomerulus -White cell cast= acute pyelonephritis -Hyaline casts= not pathognomonic for anything -Muddy brown casts= ATN -Fatty casts= nephrotic syndrome -Protein = kidneys -WBCs = infection Upper tract imaging= CT abdomen/pelvis
Albumin in proteinuria
Pathognomonic of CKD
Increases BEFORE the GFR drops
Overflow proteinuria (paraproteins)
Monoclonal gammopathies Myeloma Amyloidosis Hemoglobinuria Myoglobinuria
Glomerular proteinuria
Pregnancy Lupus IgA Minimal change dz Malignancy Familial
Tubular proteinuria
Drugs
Toxins
Fanconi syndrome
Diagnosis of CKD
GFR < 60 mL/min for 3 or more mos (if shorter it is acute)
Albuminuria > 30 mg
Anatomical d/os
Abnormal urine sediment (on repeated labs)
-Hematuria, RBC casts
Electrolyte or tubule disorders
Hx of kidney transplantation or donation
Stage I CKD
Kidney damage with nl or increased GFR
GFR greater than or equal to 90
Dx/tx of underlying condition and comorbidities
Stage II CKD
Mild
GFR 60-89
Estimate the rate of progression
Stage III CKD
Moderate
GFR 30-59
Evaluate and treat complications
Stage IV CKD
Severe
GFR 15-29
Prepare for renal replacement therapy
Stage V CKD
Kidney failure
GFR <15 or dialysis
Dialysis or transplantation if uremic
Causes of CKD
DM HTN Meds Glomerulonephritis Trauma AKI
Diabetic nephropathy
MCC of ESRD in the US High GFR Microalbuminemia Frank proteinuria Decline in GFR Typically diabetic for >10 yrs Other end organ damage is common
Tx of diabetic nephropathy
Strict glycemic control and tx of HTN
BP goal of <130/80
ACE and ARBs used in early stages as they carry some renal protective benefit
Tx of CKD
Attempt to slow progression of dz BP < 130/80 HgbA1c <7.0% LDL <100 mg/dL Tobacco cessation, wt control ACE or ARB, esp in DM or those with proteinuria Avoidance of nephrotoxic agents
Prognosis of CKD
Albuminuria is most predictive
Albuminuria occurs BEFORE a drop in GFR
GFR less than or equal to 15= kidney failure, but no dialysis until sx occur
ESRD
Most pts do not develop sx until late in dz and often nonspecific
-Fatigue, malaise, insomnia, HA
-Anorexia, metallic taste, hiccups, nausea
-Pruritis
Signs include:
-Cachexia, wt loss, altered mentation, asterixis, foamy urine
-In severe cases, pericardial rub
Renal artery stenosis
Caused by atherosclerotic occlusive dz (80-90%), fibromuscular dysplasia, HTN, CKD, DM, smoking
HTN refractory to multiple meds
Pulmonary edema with poorly controlled HTN
Increased BUN-Cr with significant renal ischemia
Audible abdominal bruit on affected side
AKI with starting of ACE/ARB is often how you diagnose
Dx of renal artery stenosis
Doppler u/s
CTA
MRA
Gold standard diagnostic= renal angiography
Tx of renal artery stenosis
Antihypertensive meds
Angioplasty with or without stenting
Fibromuscular dysplasia
Seen almost exclusively in women under 40
Treatment- percutaneous transluminal angioplasty and is often curative
Autosomal dominant polycystic kidney dz
MC genetic dz in US Commonly found at 30-40 yoa with new-onset HTN Within a family, there are variations in age of presentation, progression of dz Clinical findings: -Hematuria -Abdominal pain -Central or abdominal enlargement --Similar to PCOS presentation -HTN
Diagnostic criteria for autosomal dominant polycystic kidney dz
Renal u/s after age 30
Associated hepatic, splenic, pancreatic cysts
Associated aneurysm in Circle of Willis, evaluate for HA
Renal calculi are common
Aggressive tx of HTN may slow progression of the dz
At end stage, transplant, dialysis, or medical management
Dietary risks for nephrolithiasis
High sodium
Protein
Oxalates
Purines
What are the types of kidney stones?
Calcium oxalate, calcium phosphate= MC
Struvite= infection
Uric acid= radiolucent, not seen on KUB
Cystine= genetic, rare
S/sx of nephrolithiasis
Renal or ureteral colic, intermittent, cannot sit still
-Back pain, abdominal pain, flank pain
-Radiates to groin (testicle, labia) = lower ureter/UVJ
Nausea, vomiting, gross or microscopic hematuria
Imaging for nephrolithiasis
Gold standard= spiral CT without contrast
May demonstrate hydronephrosis
-Distention of the renal calyces and pelvis with urine d/t obstructive outflow
Organisms of pyelonephritis
Gram negs MC E. coli Proteus Klebsiella Enterobacter Pseudomonas
S/sx of pyelonephritis
Fever Rigors N/V CVA tenderness Frequency Urgency Burning Hematuria Possible sepsis with shock
Labs for pyelonephritis
Leukocytosis with left shift Blood cx may be positive Pyuria Bacteriuria Hematuria +/- white cell casts Urine cx positive with heavy growth
Tx of pyelonephritis
Inpt- ampicillin and aminoglycoside IV initially
Outpt- FQ PO and prompt f/u
Failure to respond- kidney u/s or CT scan
Renal cell carcinoma
RF- smoking Hematuria is MC presentation Often found incidentally on radiography Flank pain/abdominal mass Metastatic sx present in 20-30% Imaging- CT abdomen/pelvis, workup for mets
Where is the compensatory mechanism when the primary illness is in ventilation?
Kidneys
Where is the compensatory mechanism when the primary illness is metabolic?
The lungs
Causes of metabolic acidosis
DKA
Severe diarrhea
Renal failure
Shock
S/sx of metabolic acidosis
HA Decreased BP Hyperkalemia Muscle twitching Warm, flushed skin N/V/D Changes in LOC Kussmal respirations
Causes of metabolic alkalosis
Severe vomiting
Excessive GI suctioning
Diuretics
Excessive sodium bicarb
S/sx of metabolic alkalosis
Restlessness followed by lethargy
Dsyrhythmias
Compensatory hypoventilation
Confusion (decreased LOC, dizzy, irritable)
N/V/D
Tremors, muscle cramps, tingling of fingers and toes
Hypokalemia
Causes of respiratory acidosis
Decreased respiratory stimuli (anesthesia, drug overdose)
COPD
Pneumonia
Atelectasis
S/sx of respiratory acidosis
Hypoventilation leads to hypoxia Rapid, shallow respirations Decreased BP with vasodilation Dyspnea HA Hyperkalemia Dysrhythmias (Increased K) Drowsiness, dizziness, disorientation Muscle weakness, hyperreflexia
Causes of respiratory alkalosis
Hyperventilation (anxiety, PE, fear)
Mechanical ventilation
Conditions associated with lowered bicarb
CKD
Ingestion of methanol, ethylene glycol, excessive ASA
Diarrhea
Starvation
Conditions associated with elevated carbon dioxide
Acute respiratory failure Drug overdose COPD Morbid obesity Neuromuscular dz
Conditions associated with increased bicarb
Vomiting
Gastric suctioning
Loop or thiazide diuretics
Anion gap
The difference between measured cations and anions in serum
(Na - (Cl + HCO3))
Used in diagnosis of metabolic acidosis
Nl anion gap acidosis= HCO3 loss
Elevated anion gap acidosis = generation of new acid
-Ketoacids, lactic acid, ingestions
Causes of normal anion gap acidosis
Addisons
Bicarb loss
Chloride excess
Diuretics
Formula for urine anion gap
(Na + K) - Cl
Cause of increased urine anion gap
Renal causes increased urine HCO3
Cause of decreased anion gap
GI causes increased urine NH4 excretion
What anion gap levels are consistent with renal issues like renal tubular acidosis when kidneys cannot properly excrete ammonia?
> 20 mEq/L
What is the source most likely to be when the urine anion gap is zero or negative, but the serum anion gap is positive?
GI (diarrhea or vomiting)
Causes of high anion gap metabolic acidosis
Lactate
Toxins
Ketones
Renal
What does the MUD PILERS acronym stand for?
Methanol, metformin Uremia DKA (or alcoholic or starvation ketoacidosis) Paraldehyde, propylene glycol Infection, iron, isoniazid Lactic acidosis Ethylene glycol Rhabdo Salicylates
Other tests to consider to find root cause of high anion gap metabolic acidosis
Lactate (LA) Glucose (DM) Beta-hydroxybutyrate (DM, starvation) BUN/creatinine (Renal failure) Urine ketones (DKA, starvation) Serum levels of: -Methanol -Ethanol -Acetaminophen -Salicylates -Ethylene glycol
Osmolar gap
This is a clinical aid to evaluate the difference between the measured osmolality and the calculated serum osmolarity
Osmolar gap > 25 suggests methanol or ethylene glycol poisoning
Nl serum osmolality
275-295 mosm/kg
What occurs with increased aldosterone, leading to Na retention
Primary hyperaldosteronism
What occurs with increased ADH that leads to water retention?
SIADH
Hyponatremia
Serum Na < 135 mEq/L
Reflects excess water retention rather than Na deficiency
Hypo-osmolar, volume excess, edema forming states
SIADH, pituitary mass, meds (SSRI, SNRI)
Psychogenic polydipsia
Sx of hyponatremia
HA Lethargy N/V Disorientation Seizures Coma
Management of acute hyponatremia
Restrict water intake
Correct Na balance slowly (1-1.5 mEq/L/hr)
Severe sx: 100 cc 3% NaCl
Mild to moderate sx: 3% NaCl at 0.5-2 cc/kg/h
Management of chronic hyponatremia
Goal is to prevent central pontine myelinosis = iatrogenic cerebral osmotic demyelination
Chronic means known duration >48 hrs
Minimum 4-8 mmol/L per day
Max 10-12 mmol/L/day or 18 mmol/L/48 hr
For pts at high risk max 8 mmol/L/day
High risk: alcoholics, those with VERY low serum sodium levels, concomitant hypokalemia, liver dz, and malnutrition
Lab findings of SIADH
Serum Na down
Urine Na up
Urine osmolality up
Serum osmolality down
PE of SIADH
BP elevated
Pos edema
Tx of SIADH
Water restriction
Treat underlying dz
Induce DI by giving demeclocycline
Sx of DI
Polydipsia, polyuria
Labs of DI
Neg urine glucose
Nl serum glucose
Dx of DI
Water deprivation test: they continue to pee dilute urine despite no water
Then give ADH: it gets better= central DI
If not = nephrogenic DI
Tx for central DI
DDAVP
Tx of nephrogenic DI
HCTZ, if due to lithium toxicity, reverse cause
Hypernatremia
Serum Na > 145 mEq/L
Euvolemic hypernatremia
Renal losses, DI, lithium toxicity
Hypovolemic hypernatremia
With urine Na < 20: GI loss, sweating, burns
With urine Na > 20: loop diuretics, laxative abuse
Hypervolemic hypernatremia
Primary aldosteronism
Bicarb infusion or pushes
Hypertonic dialysis
Cushing’s
Sx of hypernatremia
Lethargy
Irritability
Weakness
Thirst
Management of hypernatremia
Slow correction over 48 hrs
Hypovolemia: isotonic nl saline
Euvolemia: 5% dextrose IV or water ingestion
Hypervolemia: 5% dextrose IV, loop diuretics, possibly dialysis
What can hypokalemia result from?
Insufficient intake Increased excretion (diuretics, hyperaldosteronism) Shift from extracellular to intracellular space GI losses via vomiting or diarrhea
