Renal Flashcards

Question

Staging of CKD

Answer 1

Chronic Kidney Disease * Stage 1: **Normal** GFR ≥ 90mL/min/1.73m2 * either persistent albuminuria or known structural or hereditary renal disease * Stage 2: **Mild** GFR 60-89 mL/min/1.73m2 * Stage 3: **Moderate** GFR 30-59 mL/min/1.73m2 * Stage 4: **Severe** GFR 15-29 mL/min/1.73m2 * Stage 5: **Kidney Failure** GFR \< 15mL/min/1.73

Answer 2

dx: **GFR \< 60mL/min/1.73m2** for **3 months** or any of the following: * _albuminuria_: urine albumin: creatinine ratio **\>30mg/day** * _proteinuria_: urine protein: creatinine ratio **\> 0.2** * _hematuria_ * _structural renal abnormalities_ ( solitary kidney, hx of abnormal renal histology hx of renal transplant)

Answer 3

* Diabetes = **MOST COMMON CAUSE (30%)** * HTN (25%) * chronic glomerulonephritis (15%) * interstitial nephritis, polycystic kidney disease, obstructive uropathy

Answer 4

* **Pruritus = common**, but difficult to tx * _Cardio_: HTN → caused by salt and water retention → decreased GFR = stimulation of RAAS → increased BP → CHF due to volume overload, HTN, anemia → pericarditis * _GI_: (usually due to uremia) nausea, vomiting, loss of appetite * _Neuro_: lethargy, confusion, tetany → (due to **hypocalcemia**), uremic seizures, peripheral neuropathy * _Heme_: normocytic, normochromic anemia (secondary to **deficiency of erythropoietin**) * bleeding secondary to platelet dysfunction→ platelets **do not degranulate in _uremic environment_** * _Endo/Metabolic_: * Ca²⁺/Phosphorus disturbances→ decreased renal secretion of phosphate leads to **hyperphosphatemia** → decreased production of 1,25-dihydroxy vitamin D → **hypocalcemia** → **hyperparathyroidism** * hyperkalemia → decreased secretion and **acidosis** * _Fluid & Electrolyte problems_: * **volume overload**: watch for pulm edema * **hyperkalemia**: due to decreased urinary secretion * **hypermagnesemia**: secondary to reduced urine secretion * **hyperphosphatemia**: decreased clearance of phosphate * **metabolic acidosis**: due to loss of renal mass (& therefore decreased ammonia production) & kidneys' inability to secrete H⁺

Answer 5

* Dx: **GOLD STANDARD = GFR** * _urinalysis_: **waxy casts, or granular casts** → show dilation and hypertrophy of remaining nephrons * _Proteinuria_ * elevated _BUN & creatinine_ * **hyperphosphatemia & hypocalcemia** * low **_erythropoietin levels_** (due to loss of renal function) * Tests to order: CBC, chem panel (CMP), iron studies, lipid profile, urinalysis

Answer 6

* Tx: **ACEI and ARBs** → slow progression of renal dysfunction * manage the comorbidities!! : control HTN, glycemic control (A1C 6.5-7.5%), cholestrol control, tobacco cessation * **Maintain HGB at 11-12 g/dl** → Do not want to bring pt up to normal hgb levels → pro-thrombotic b/c it thickens the blood & increases mortality * **Dietary management**: protein restriction, calcium and vitamin D supplements, limit water, sodium, and potassium and phosphorus * **Need for hemodialysis or kidney transplant** * **PCV-23** * Fluid overload management: dietary salt \<2 gm/day * **GFR \> 30** → thiazide diuretics (hydrochlorothiazide, chlorthalidone) * **GFR \<30** → loop diuretics (furosemide, torsemide, bumetanide) * can use phosphorus binders to reduce hyperPTH → **calcium carbonate, calcium acetate, sevelamer, lanthanum, iron** * tx the acidosis: may reduce risk of CKD progression → NaHCO3- → goal bicarb level \>22

Answer 7

caused by secondary hyperPTH often as a result of CKD * increased phosphate due to decrease in secretion in kidneys → decreases production of 1,25-dihydroxy vitamin D (Calcitriol) → hypocalcemia → hyperparathyroidism * body then break down bones to increase serum calcium

Answer 8

* Urinary Tract obstruction that leads to the collecting system in one or both kidneys to **dilate** * _Etiology_: kidney stones (uretral), tumors, bladder outlet obstruction (BPH or prostate cancer) and sloughed off renal papillae * _S/sxs_: * usually asymptomatic * can have change **in urine output (_Difficulty urinating/hesitancy)_, HTN, hematuria**, and CVA tenderness, pain in the side, abdomen, or groin * _Dx_: * UA→often benign but may show hematuria or elevated pH * may have a **palpable abdominal or flank mass** caused by an enlarged kidney * Labs: may have increased serum creatinine * U/S: **initial imaging that you should do → will show dilation of the collecting system in one or both kidneys** * CT Scan: indicated for those with flank pain and suspected nephrolithiasis or in pts whom visualization of the ureters is needed * _Tx_: * **Removal of obstruction** → rapidly reversible if removed quickly, can lead to UTIs and possible ESRD

Answer 9

**Autosomal Dominant** → mutations of *PKD1* or *PKD2* → causes 10% of ESRD * _formation & enlargement of kidney cysts_ (cysts also common in the liver (most common), then spleen and pancreas * _Pathophys_: * vasopressin (ADH) stimulates cytogenesis and eventually leads to ESRD over time * _S/sxs_: **renal → abdominal pain & flank pain**, nephrolithiasis, UTI and hematuria * ~10% of pts **have brain aneurysms** (so be concerned about headache complains) * **abdominal fullness** * mitral valve prolapse and L ventricular hypertrophy * _Dx_: **U/S → shows fluid filled cysts**, CT scan will show large renal size and thin walled cysts * **need to U/s rest of direct family members** * _Tx_: no cure, only supportive to ease sxs * control HTN \<130/80 with use of **ACE-I & ARBs** * infx should be treated quickly/vigorously with abx * dialysis or transplant should be considered when renal insufficiency becomes life threatening

Answer 10

aka renovascular HTN * **HTN caused by renal artery stenosis** in one or both kidneys * \*\*\*MOST COMMON cause of _secondary HTN_\*\*\* * _Pathophys_: decreased renal blood flow leads to activation of RAAS * _Etiologies_: **atherosclerosis** = most common in elderly, **fibromuscular dysplasia** = most common cause in women \<50 * _S/sxs_: * suspect in pts with **headache & HTN \<20 years** * or **\>50 years, severe HTN** or **HTN** resistant to 3+ drugs * or **abdominal bruits** * or it pt develops **AKI after the initiation of ACE-I therapy** * _Dx_: * non-invasive option: **CT angiography**, MR angiography, Duplex doppler (duplex doppler = less sensitive, specific) * **Renal Catheter Arteriography = GOLD STANDARD and definitive** → revascularization can be performed during the same procedure if stenosis is found (not used in pts with renal failure) * _Tx_: * **Revascularization = definitive management** * **angioplasty with stent** → performed if creatinine \>4.0, increased creatinine with ACE-I tx, or \>80% renal stenosis * Bypass if angioplasty is not successful * Medical Management: * **ACE-I or ARBs** (BUT these are contraindicated in pts with bilateral stenosis or solitary kidney b/c can cause AKI due to ischemia

Answer 11

End Stage Renal Disease * Stage 5 CKD → GFR \<15, complete loss of kidney function for more than 3 months * **Most Common Cause = DM** * _Dx_: * **GFR \<15mL/min/1.73m2 for ≥3months** * low EPO levels * metabolic acidosis * **increased potassium, phosphate, and PTH** * **low calcium, sodium, bicarb** * “_Waxy” cats_ **with low urine flow** * _Tx_: * **Dialysis & kidney transplant** * Manage co-morbidities: * bring HGB up to 11-12 (no higher or else possibility of clots) * **dietary management**: protein restrictiion, Calcium and Vitamin D supplements, limit water, sodium, potassium, and phosphorus * **ACE-I & ARBs** = slow progression of renal dysfunction * **Loop diuretics**: preferred addition to the management of edema associated with HTN due to ESRD * **Pneumococcal vaccine**

Answer 12

End stage renal disease * _S/sxs_: * **pruritus** * **HTN,** may have A/B nicking, copper wire changes on retina * **S4 heart sound** * Kidneys affected by ESRD cannot regulate levels of electrolytes → **sodium excess** = retention of water * **potassium excess** = abnormal heart rhythm, can lead to cardiac arrest * **magnesium deficit** = can affect heartbeat and cause changes in mental state * _Hormones_: cannot absorb calcium and bones become weak and may break (**renal osteodystrophy)** * **erythropoietin production decrease** = normochromic, normocytic anemia * _Enzymes_: kidneys affected by ESRD respond to lower GFR by making too much renin → keeps blood pressure levels high → difficult to tx

Answer 13

* shortened QT * ST depression * Peaked T wave

Answer 14

* decreased T-wave amplitude * ST depression * increased U-wave amplitude

Answer 15

* _Urine potassium \< 20mmol/L_ * metabolic acidosis: diarrhea, laxative * _Urine potassium \> 20 mmol/L_ * *metabolic acidosis*: * proximal RTA, or distal RTA * *Metabolic Alkalosis + Normal or Low BP* 1. Low urine chloride (**\<20)** 1. vomiting 2. High Urine Chloride **(\>20)** 1. Lasix 2. thiazide 3. Mg depletion 4. Bartter's 5. Gitelman's * *Metabolic Alkalosis + High BP* * increased renin + increased aldosterone: * renal artery stenosis or renal tumors * decreased renin + increased aldosterone * primary aldosteronism * decreased renin + decreased aldosterone * Cushings * liddles * apparent mineralocorticoid excess (licorice, drugs) * MR mutation

Answer 16

**identify and tx underlying causes** * NaHCO₃^- indicated when: * **renal dysfunction**→ not enough HCO3- is regenerated * **Severe acidemia:** pG \<7.10 * goal: increase HCO3- by 10mEq/L; and ph\> 7.2 * **½ of the amount is given over 3-4 hours; then remainder given over 8-24 hours** * \*\*\*\*1mEq/kg/dose and monitor\*\*\*

Answer 17

used to treat metabolic acidosis * can be used with loop diuretics to avoid too much fluid (fluid overload) * indicated when: * **renal dysfunction** → not enough HCO3- regenerated * **severe acidemia**: pH\<7.10 * **½ of the amount is given over 3-4 hours; then remainder given over 8-24 hours** * **one amp is 50mL (or 50mEq)** * **can give up to 3 amps + 1L D5W**

Answer 18

used to tx metabolic acidosis * helpful when the acidosis is coupled with hypoK+ * **be cautious with renal impairment → needs to be avoided if pt has hyperK+ (can cause increased HyperK+)**

Answer 19

* pts rarely have symptoms due to alkalemia * sxs often related to volume depletion * muscle cramps * dizziness depending on position * HypoK+ → muscle weakness, polyuria, polydipsia * **Tx**: **tx the underlying cause** * i.e. meds, **citrate** containing products (K-citrate used to tx metabolic acidosis), or acetate in parenteral nutrition → causes HCO3- levels to rise * alkalosis caused by vomiting, NG suction, or diarrhea +/- urinary Cl- (\<25mEq/L) → **saline infusion** * **acetazolamide** (carbonic anhydrase inhibitor) → reduces HCO3- concentration * \*\*\*\*\*\***Hemodialysis** or **HCl infusion** for life-threatening metabolic alkalosis\*\*\*\*\*\*

Answer 20

represents ventilation failure or impaired control of ventilation * hypoxemia + hypercapnia * severe, acute respiratory acidosis = * HA, blurred vision, restlessness and anxiety, tremors, somnolence, and/or delirium * Tx = identify cause and tx that: * opiate/opioids → **naloxone** * acute bronchospasm/asthma → bronchodilators * assisted ventilation and mod-severe acidosis → BiPAP * NOTE: NaHCO3 may actually worsen acidemia due to increased CO2 generation so do NOT use this * Goals: * careful monitoring of pH * maintain oxygenation * improve alveolar ventilation

Answer 21

represents hyperventilation * sxs: irritability of central and peripheral nervous system * light headedness, altered consciousness, cramps, syncope * s**evere cases: HypoPhos** shifts from ECF to ICF * tx: identify cause and tx accordingly * f**or mild-moderate** severity in spontaneously breathing pts → no specific tx * **severe alkalosis**: * rebreathing * rebreathing mask, or paper bag * mechanical ventilation * high level sedation or paralysis is a good option

Answer 22

Na+, Cl-, HCO3-

Answer 23

K+, Mg2+, PO₄^2-, SO₄^2-

Answer 24

* at least 1-2 L of NS as rapidly as possible (bolus) * restores tissue perfusion * fluid replacement is continued at rapid rate until clinical signs of hypovolemia improve

Answer 25

* Na+ \<135 * Hypertonic hyponatremia (Osmolarity \>**300 mOsm/L**) * Hypotonic Hyponatremia (i.e. dilutional→ **\<275 mOsm/L**) * hypervolemic * gain of both water and sodium * water \>\>\>\>\> sodium * euvolemic * gain of water (ECF volume is normal) * total body water \>\>\>\>normal total Na+ * hypovolemic * loss of both water and sodium * sodium \>\>\>\>\>water

Answer 26

osmolarity \> **300 mOsm/L** associated with **severe hyperglycemia** 60mg/dL of Glc \>200 = 1mEq/L reduction of Na+ tx: **Tx the hyperglycemia** → insulin

Answer 27

Hypotonic hyponatremia (osmolarity \<**275 mOsm/L**) * body gains **excess Na+ and Water** * but Water \>\>\>\>\>Na+ * Causes: **HF, cirrhosis, nephrotic syndrome** * tx: *Fluid & Na+ restriction (i.e. 2 gm/day)* * optimize the underlying disease state * diuretics * increase the intravascular oncotic pressure (albumin) * pulls fluid of out intracellular compartment

Answer 28

aka isovolemic hyponatremia hypotonic hyponatremia (osmolarity \<**275 mOsm/L)** ECF volume is normal * **have excess water → total body water \>\>\>\>normal total Na+** * **water intoxication** * causes: SiADH (too much ADH secreted), Polydipsia, decreased water secretion * carcinomas (small cell lung cancer) * CNS disorders → stroke, meningitis, trauma * medications: SSRIs, NSAIDs, antipsychotics, sulfonylureas * Tx: * _Non-acute (Na \>115mEq/L and asymptomatic_: * **fluid restriction**, possible chronic therapy * _Acute (Na \<115 mEq/L and/or sxs)_: * **3% NaCl infusion** * +/- diuretics to correct fluid accumulations * fluid restriction → 1000-1200mL/day * \*\*\*\*\*\***no more than 12 mEq/L/24 hours (0.5mEq/hour**)\*\*\*\*\*\* * can cause osmotic demyelination syndrome → myelin cells swell/shrink and die

Answer 29

hypotonic hyponatremia (osmolarity \<**275 mOsm/L)** decreased ECF volume * decrease in both Na+ and Water * deficit of Na+ \>\>\>\>\> deficit of water * Causes: * diuretics (thiazides), diarrhea, vomiting, NG suction * Treatment: **NS @ 300ml/hr until improvement in symptoms** * \*\*\*\*\*DO NOT CORRECT SODIUM LEVELS \>12mEQ/L/24 HOURS\*\*\*\*\*\*

Answer 30

* *Hypernatremia = \>145 Na+* * **Hypovolemic Hypernatremia** * **loss of water \>\>\>\>\> sodium** * *Isovolemic Hypernatremia* * *water loss only* * **Hypervolemic Hypernatremia** * **body has excess sodium and water** * **sodium \>\>\>\>\>\>water**

Answer 31

* S/sxs: polyuria, polydipsia, confusion, obtundation, stupor, tremor, rigidity, coma * causes (free water deficit): * dehydration * incapable of obtaining water * fever/infx/sweating/burn pts * diabetes insipidus * hyperglyuria/osmotic diuretics * excessive sodium intake & cushing sx

Answer 32

* when water loss \>\>\>sodium loss * causes: diarrhea, sweating, diuretics * tx: d/c diuretics or laxatives * **if symptomatic**: initially 200-300ml/hr with NS (to achieve hemodynamic stability) * replace free water deficit: D5W, ½ NS or a combo * **asymptomatic**: D52, ½ NS, or a combo

Answer 33

aka euvolemic hypernatremia water loss only * causes: * **Diabetes insipidus**: * central DI = decreased ADH production * Nephrogenic DI = decreased renal response to ADH * drug induced DI: * aminoglycosides, Ampho B, cochicine, demeclocycline (used to tx chronic euvolemic hyponatremia) * Tx: * _initially_: **D5W** (replace free water) * _chronically_: * for central DI: **desmopressin** (DDVAP) b/c it is a synthetic analog to ADH → act on the V2-receptors of collecting duct → water reabsorption * for nephrogenic DI: **NSAIDs [can cause euvolemic hyponatremia] (indomethacin, IBU, naproxen, diclofenac, ketoprofen) and thiazides**

Answer 34

NSAIDs reduce renal prostaglandins and prostaglandins inhibit the action of ADH so NSAID use can increase action of ADH and cause increased water reabsorption

Answer 35

synthetic analogue of ADH Act on V2-receptors at the collecting duct → reabsorption of water used to tx central diabetes insipidus → the underlying pathophys behind isovolemic hypernatremia

Answer 36

body has excess sodium and water sodium \>\>\>\> water * causes: * renal failure * Tx: * replace intravascular deficit if necessary (use D5W, ½ NS or a combo) * loop diuretics (if making urine) (increases sodium excretion) * hemodialysis

Answer 37

When to tx? \<3.5 mEq/L and/or pt is symptomatic * treatment: * oral: **K-chloride, KPO₄, K-acetate, K-citrate, k-gluconate** * IV: if \>10 mEq/L should be monitored via telemetry * other: diuretic induced (**spironolactone- K+ sparing diuretic**) * correct hypomagnesemia * \*\*\*\*low magnesium makes body resistant to K+ replacement, so tx mg deficiency first or concurrently\*\*\*\*\* * correct acid-base imbalance

Answer 38

* _Symptomatic (urgent/emergent_) * **IV calcium** to stabilize the heart membrane * **insulin +/- glucose/dextrose** to temporarily push K+ back into the cell * **albuterol** to also temporarily push K+ back into the cell * **Sodium bicarb** to be considered to tx acidosis * **Eliminate Source**: IV, total parenteral nutrition (TPN), tube feeds, oral supplements, K sparing diuretics * _Symptomatic_: * **sodium polystyrene sulfonate (Kayexelate)** → binds potassium, slower onset, but duration of 4-6 hours (constipation though…) * **Loop diuretics** (lasix) * _Asymptomatic_; * eliminate source * kayexelate (sodium polystyrene sulfonate) → binds potassium * loop diuretics

Answer 39

* **potassium \<3.5 mEq/L** * _Etiology:_ * increased urinary/Gi losses * diuretic therapy, vomiting, diarrhea; renal tubule acidosis * increased intracellular shifts * metabolic acidosis, beta-2 agonists, hypothermia, insulin, aldosterone * hypomagnesemia * decreased intake→ rare * _S/sxs_: * neuromuscular: severe muscle weakness, rhabdomyolysis * nephrogenic DI: **polyuria** (affects renal concentrating ability), cramps, n/v, ileus (obstruction of ileum * cardiac: palpitations, arrhythmias * ***no change in mental status*** * _Dx_: * BMP: potassium \<3.5mEq/L, *magnesium, glucose, and bicarb should be ordered in work up* * Spot Urine K \> 20 mmol/L (renal cause) * Spot Urine K \< 20mmol/L (non-renal cause) * **ECG findings**: _T-wave flattenedfollowed by a prominent_ **_u-wave_** * _Tx_: potassium replacement→ KCl oral if possible, IV KCl if rapid/severe tx needed * potassium sparing diuretic (**spironolactone, amiloride)** * check for hypomagnesemia (need to correct for this 1st or concurrently) * \*\*\*Use non-dextrose IV solutions b/c dextrose will cause spike in insulin release which will cause more K to shift into the cells \*\*\*

Answer 40

**serum potassium \> 5-5.5mEq/L** * Etiology: * **decreased renal excretion: acute/chronic renal failure** * decreased *aldosterone* → hypoaldosteronism, adrenal insufficiency * _Meds_: K+ supplements, K+ sparing diuretics (thiazides, spironolactone, amiloride), **ACEI/ARBs**, digoxin, beta-blockers, NSAIDs, cyclosporin * Cell lysis → rhabdomyolysis, hypovolemia, thrombocytosis, tumor lysis syndrome * K redistribution → metabolic acidosis * _S/sxs_: * **neuromuscular**: weakness (progressive ascending), fatigue, paresthesias (tingling), flaccid paralysis * cardiac: palpitations and cardiac arrhythmias * GI: abdominal distention, diarrhea * _Dx_: * ECG: **peaked T-waves, prolonged QRS, St depression** * BMP: potassium \> 5.0 mEq/L, *glucose and bicarb part of the workup +/- CBC (hemolysis)* * _Tx_: repeat blood draw to ensure that increased K isnt from hemolysis (since venipuncture may cause this) * **IV Calcium Gluconate** → stabilize the cardiac membrane → only for severe symptoms, K \>6.5, + significant ECG findings * → **insulin with glucose/dextrose** → insulin shifts K+ intracellularly * **Kayexalate (sodium polystyrene sulfonate)** → enhances GI excretion of K+, lowers total K+ * **SABA**: albuterol (4-8x dosing for asthma) * **loop diuretics;** dialysis if severe

Answer 41

* **serum sodium \>145 mEq/L** * caused by increased free water loss, hypotonic fluid loss, or hypertonic sodium gain * _Etiology_: **diabetes insipidus**, diarrhea, sweating, burns, fever, insensible loss * → infants, elderly, debilitated pts or impaired thirst mechanism → water intake decreased * _S/sxs_: PRIMARILY CAUSED BY SHRINKAGE OF BRAIN CELLS → dehydration * **thirst = most common initial sx** * confusion, lethargy, disorientation, fatigue, N/V, muscle weakness, *seizures, coma, brain damage resp. arrest* * _PE_: **dry mouth, mucus membranes, decreased skin turgor**, tachycardia, hypotension * _Dx_: **serum studies** → serum Na, urine osmolarity, serum osmolarity, assess volume status * _Tx_: **hypotonic fluids**: pure water oral, D5W, 0.45%NS, * isotonic fluids if hypovolemic to replenish volume then *hypotonic fluids* * if Central **diabetes insipidus → desmopressin (synthetic analog to ADH)** * renal diabetes insipidus → **NSAIDs** (constrict afferent renal arteriole and reduce GFR) * **rapid correction (\>0.5mEq/L.hr)** → can results in **_Cerebral edema_**

Answer 42

**serum sodium \<135 mEq/L** * due to _increased free water_ * clincially significant → hypotonic hyponatremia * _etiology_: * hypertonic hyponatremia → due to *hyperglycemia or mannitol infusion* * Isotonic Hyponatremia → lab error due to hyperproteinemia or hypertrigliceridemia * _Hypotonic Hyponatremia_ → * **hypovolemic** → renal volume loss (diuretics, ACEI); extraneal volume loss → GI loss (diarrhea & vomiting), burns, fever * **Isovolemic:** SIADH, hypothyroidism, adrenal insufficiency water intoxication, MDMA, tea and toast syndrome * **hypervolemic**: edematous states → CHF, nephrotic syndrome, cirrhosis * _S/sxs_: **primary caused by cerebral edema** → confusion, lethargy, disorientation, fatigue, N/V, cramps, *Seizures, coma, respiratory arrest* * _PE_: * **hypervolemia** → edema, JVD, HTN; decreased HCT, serum protein, BUN:creatinine * **hypovolemia→** poor skin turgor, dry mucus membranes, flat neck veins, hypotension; increased hct, serum protein, BUN:creatinine ratio \>20:1 * _Dx_: * 3 steps: 1. measure serum sodium 2. serum osmolality (**275-295 mOsm/kg**) 3. assess volume status (if hypotonic/decreased osmolality)

Answer 43

* **causes rapidly progressive Glomerulonephritis (nephritic syndrome)** * _anti-glomerular basement membrane_ * _presentation_: * lungs/kidneys hemorrhage * teenagers & \>50 years * rapidly progressive→ _fatal_ * _Pathology:_ * antibodies against the glomerular basement membranne * often associated with crescent formation * _Tx_: * **cyclophosphamide + corticosteroids + plasmapheresis** * due to high fatality → START RX while waiting for dx

Answer 44

* _Presentation_: * E.coli O157:H7 (foodborne), Salmonella, etc. → undercooked meat consumption * *bloody diarrhea that has resolved* * **fever; low platelets; AKI** * Dx: * often via serum assays * _Treatment_: symptomatic manage,ent * HUS may require dialysis, 10% death rate

Answer 45

* type of nephritic syndrome → **cause of _rapidly progressive glomerulonephritis_** * _Presentation_: **hematuria + signs of necrotizing small vessel vasculitis** (diffuse skin lesion, lung hemorrhage, sinusitis, etc.) * _Tx:_ aggressive tx with steroids, cyclophosphamide or rituximab * **plasmapheresis** → severe disease

Answer 46

* _S/sxs_: usually hx of lupus * SLE more common in female AA population * **proteinuria, hematuria**, + **elevated creatinine** * _Tx_: dependent on biopsy classifications

Answer 47

Rhabdomyolysis

Answer 48

albumin * can have a false negative if proteinuria composed of light chains * → will be detected in protein precipitation test aka **sulfosalicyclic Acid (SSA)**

Answer 49

albumin * can have a false negative if proteinuria composed of light chains * → will be detected in protein precipitation test aka **sulfosalicyclic Acid (SSA) → Myeloma**

Answer 50

\< 0.2 or 200 aka SPOT urine protein/SPOT urine creatinine

Answer 51

\<200mg/day

Answer 52

30-300mg/g

Answer 53

when the “nephritis” is causing an AKI that is rapidly progressive over days to weeks * _Nephritis_: * RBC casts * proteinuria \<3.5g

Answer 54

Non-oliguria: \>400mL/day Oliguria: 100-400 mL/day Anuria: \<50mL/day

Answer 55

A: severe metabolic Acidosis E: Electrolyte Problems (Hyperkalemia) I: Intoxication (Antifreeze) O: Overload of fluids U:Uremic symptoms (pericarditis, altered mental status)

Answer 56

3-4+ proteins, RBCs and RBC casts, granular & epithelial casts, oval fat bodies

Answer 57

**GFR \<30 ml/min/1.73m2 \*CKD stage 4-5)**

Answer 58

* Advantages: * less sxs f * continuous theraoy * fewer dietary restrictions * needleless * home therapy * flexibility with schedule * easy night-time therapy * easier travel * Disadvantages: * daily (as opposed to 3 times a week) * training required * weight gain, sugar-load * need for clean space in room for PD and supplies * peritonitis risk (though balanced by bacteremia risk of HD)

Answer 59

15 years more

Answer 60

tacrolimus and cyclosporine (CSA) tacrolimus can cause kidney injury * SE: DM, HTN, hypercholesterolemia

Answer 61

generally okay to keep going as long as: * K controlled * creatinine increases \<20-30% within 6-8 weeks at start * no abrupt AKI * no other SEs (ACEi → cough, angioedema, etc. so can use an ARB instead)

Answer 62

* Urine Na: **\>40mEq/L** * urine osmolality: \<350 * BUN/Creatinine Ratio: 10:1 * FeNa: \>2% * FeUrea: \>35%

Answer 63

to calculate expected pCO₂ * Expected pCO₂ = (1.5 x bicarb) + 8 +/- 2 * if pCO_{2 = higher than expected → additional respiratory acidosis} * if PCO_{2 = lower than expected → additional respiratory alkalosis}

Answer 64

urine albumin: creatinine ratio **\>30 mg/g (per day)**

Answer 65

urine protein: creatinine ratio **\>0.2g/g** or **\>200mg/g**

Answer 66

along afferent arteriole that detect blood pressure if BP = low → secrete renin and activate RAAS system

Answer 67

Decr ADH in Central Diabetes Insipidus (neuro issue) Urine osmo \<300, corrects w/ ADH administration Decr sensitivity to ADH in Nephrogenic Diabetes Insipidus (renal issue) Urine osmo \<300, does NOT correct w/ ADH **Hypernatremia will only occur if water intake is inadequate**

Answer 68

Insensible losses GI losses Fluid shift into cells Urine osmo \>800 Urine Na \<10 **Hypernatremia will only occur if water intake is inadequate**

Answer 69

Causes K excretion in principal cells of CD and K reabsorption in intercalated cells of CD

Answer 70

urine [K+] \> 20 mmol/L = renal cause urine [K+] \< 20 mmol/L = nonrenal cause

Answer 71

GFR: \< 60 mL/min = CKD \< 30 mL/min = referral to nephrology \< 20 mL/min = eligible for transplant listing \< 10 mL/min = dialysis

Answer 72

Stage 1: Incr SCr by **0.3 mg/dL x 48 hrs** or **+50% x 7d**, UOP \<0.5 mL/kg x \>6h Stage 2: UOP \<0.5 mL/kg x \>12h Stage 3: UOP \<0.3 mL/kg x \>24h or anuria \>12h

Answer 73

1st line therapy for HTN in early CKD as they "tell kidneys to take a break & not filter so hard" Will cause slight incr in SCr. Expected and ok as long as \<30% and proteinuria is improving. Watch K as ACEi/ARB can increase **Do not use ACEi & ARB together d/t incr risk of AKI, hyperkalemia, hypotension**