Lecture 13 (Renal)-Exam 5 Flashcards

Question

PKD-Complication Treatment * Pain: * Hematuria:

Answer 1

* Pain – bed rest, analgesics * Hematuria – usually due to rupture of cyst into the renal pelvis, but could be a stone or UTI – hydration and bed rest

Answer 2

* Renal Infection – flank pain, fever, leukocytosis – CT may show increased cyst wall thickness if cyst infected. Difficult to treat – needs a fluoroquinolone or Bactrim. Treatment may require IV abx followed by long-term PO abx. * Nephrolithiasis – increase hydration to 2-3 L/day to prevent precipitation of stones

Answer 3

* HTN – 50% will be hypertensive on presentation. Cyst-induced ischemia appears to cause activation of the renin-angiotensin system. Use an ACE inhibitor or an ARB * Cerebral Aneurysms – 10-15% will have arterial aneurysms in the circle of Willis. Screening recommended only if family hx positive, undergoing elective surgery, or in a high-risk profession (pilot). * Other – diverticulosis, aortic aneurysms, mitral valve prolapse

Answer 4

* Vasopressin receptor antagonists decrease the rate of change in total kidney volume and eGFR decline. * Tolvaptan is FDA approved for the treatment of autosomal dominant polycystic kidney disease. * Encourage the patient to drink at least 2 L of water daily. * Treatment of HTN and a low-protein diet may slow the progression – maybe.

Answer 5

* Congenital & typically asymptomatic, so look for it in neonates * 1 in 1000 have some type of renal fusion * Horseshoe kidney is the most common * Fused renal mass almost always contains two excretory systems and therefore two ureters

Answer 6

* Renal mass may be entirely on one side or divided equally on the flanks * May remain in the pelvis and have alternate blood supply. * Seen quite frequently in Turner syndrome, Trisomy 13, 18, 21 * Complications - stones, pyelonephritis, increased risk of renal cancer

Answer 7

* Most have no symptoms * Some develop ureteral obstruction (ureteropelvic junction obstruction) * GI symptoms that mimic peptic ulcer, cholelithiasis or appendicitis may be observed

Answer 8

* Infection is a risk if ureteral obstruction and hydronephrosis or calculus develops * UA normal unless UTI * Renal function normal unless disease coexists in each of the fused renal masses

Answer 9

* CT clearly reveals * However – plain x-ray may reveal, urogram, US * Prone to ureteral obstruction (UP junction-> dt urine stasis) * Hydronephrosis, stone formation, infection (pyelonephritis -> dt urine stasis)

Answer 10

No TX typically needed (if asymp-> do serial UAs) Prognosis – usually excellent

Answer 11

Replace Obligatory Fluid Losses * Sensible (measurable) = urine * Insensible (not easily measurable) = lung, perspiration

Answer 12

Replace Exceptional Losses (present pathophysiologically) * Diarrhea * Vomiting * NG tube * Drains & Fistulas * Blood * Surgical evaporative losses (exploratory laparotomy)

Answer 13

* Daily weights- reflection of fluid (scale or a lift/bed) * Monitor I & O (intake and output) and electrolytes

Answer 14

* Normal Saline 0.9% (NS) – almost isotonic * 0.45% Normal Saline (1/2 NS) * Ringer’s Lactate or Lactated Ringers (LR/ RL) – surgeons favorite * Dextrose 5% with 0.45% Normal Saline (D5W & 0.45% NS) * 5% dextrose in water (D5W) * TGH Special: House Wine (D5 1/2NS with KCl 20mEq * 3% Saline: hypertonic

Answer 15

* diabetics and people needing the free water * Should be avoided in Wernicke patient or alcoholics * Glucose oxidation is a thiamine-intensive process that may drive the insufficient circulating vitamin B-1 intracellularly

Answer 16

NG tube suctioning

Answer 17

* Lactate turns into bicarbonate – good in lactic/metabolic acidosis (counteracts it). Don’t give with High pH. * D5 sugar (solute) gets used by your body and you end up with free water w/o solute. So if theres high Na and hypovolemia – give D5W slowly to increase fluids. * Glucose in D5W 0.45 is good cause you’ve been NPO 8hrs after procedure.

Answer 18

* Osmotic Pressure responsible for water movement across cell membranes * Depends on the total number of solute particles (osmoles) dissolved in solution * Usually expressed as milliosmoles of solute per kilogram of solvent (mOsm/kg)

Answer 19

Proximal Tubule: * Fluid is isosmotic to ECF (300 mOsm): The fluid entering the proximal tubule has the same osmolarity as the extracellular fluid. Loop of Henle * Descending Limb: Water is reabsorbed (H₂O) into the surrounding medulla due to the high osmolarity of the interstitial fluid. This results in the fluid becoming more concentrated (hyperosmotic). * Ascending Limb: Here, Na⁺, Cl⁻, and K⁺ are actively transported out of the tubule without water following, creating a hypoosmotic fluid (lower osmolarity) by the time it reaches the distal tubule. Distal Tubule * Hypoosmotic Fluid (100 mOsm): The fluid entering the distal tubule is hypoosmotic due to the active transport of solutes in the ascending limb of the Loop of Henle. Collecting Duct * Permeability to H₂O Varies: The permeability of the collecting duct to water varies, which is influenced by the presence of antidiuretic hormone (ADH). * Urine Osmolarity Depends on Permeability: If the collecting duct is permeable to water (high ADH), water is reabsorbed, leading to more concentrated urine. If it's impermeable (low ADH), less water is reabsorbed, resulting in diluted urine.

Answer 20

* Serum sodium >145 mEq/L – DUE to free water loss * Causes – diarrhea, diuretics, sweating, fever, burns, **diabetes insipidus** * Infants, disabled, elderly who cannot take in adequate H20 (hot elderly syndrome)

Answer 21

* Clinical - thirst (MC initial symptom) , confusion, lethargy, fatigue, muscle weakness. If severe – seizure, coma, death. * Exam – dry mucous membranes, decreased skin turgor, tachycardia (early sign), hypotension (late sign) .

Answer 22

* Correct shock (Normal saline! or LR) * Treat underlying cause (fever, vomiting, diabetes insipidus, etc) * Replace water deficit

Answer 23

* Hypovolemic causes – either renal (severe hyperglycemia or osmotic diuretics) or extrarenal (sweating, GI or Resp loss, dehydration) * Isovolemic/euvolemic causes – diabetes insipidus (lack of ADH) * Hypervolemic – mineralocorticoid excess, hypertonic saline

Answer 24

Clinical for all forms – dependent on rapidity and severity – CNS dysfunction (confusion, lethargy, fatigue)

Answer 25

DI: inability of the kidney to concentrate urine, leading to production of large amounts of dilure urine * Central DI: Deficiency of ADH production by hypothalamus (synthesized)-pituitary (released) * Nephrogenic DI: Kidney resistance to ADH

Answer 26

Sxs: Thirst and hypotonic polyuria (3-20 L daily) Dx: * Hypernatremia * Daily urinary excretion of 3 liters or more * Low urine specific gravity <1.010 or 24hr urine osmolality < 300 mOsm (**LOW**) * Serum osmolarity (**increased** dt to increased urinary free water loss) ## Footnote Normal Urine Sodium – 20mEq/L at random; 40-220 per day Normal Urine osmolality – 50-800 at random (depending on hydration status), 500-850 mOsm/kg per day

Answer 27

Water deprivation test can be performed, but can cause severe dehydration * Differentiates from psychogenic polydipsia (PP causes dilution hyponatremia and doesn’t respond to exogenous ADH admin)

Answer 28

* Serum – sodium, urine osmolarity, serum osmolarity * Assess volume status: (**Hyperosmolality** nearly always associated with hypernatremia) * Urine sodium: Urine osmolarity (low if urine dilute – **diabetes insipidus**), (high if urine concentrated due to extrarenal cause – **dehydration**)

Answer 29

* Use hypotonic fluids in euvolemic: H2O, D5W, 0.45 NS, 0.2 NS * Use isotonic fluids if hypovolemic – NS or Lactated ringers. * Rate - >0.5 mEq/L/hr can result in cerebral edema ( do not want to go too fast)

Answer 30

* Sodium <135 (increased free water due to kidneys inability of kidneys to excrete excess water) * Symptoms include headache, vomiting, AMS, seizure * Serious symptoms caused by cerebral edema * Beware overcorrection- central pontine myelinolysis (osmotic demyelinating syndrome)

Answer 31

* Pseudohyponatremia- saline contamination, hypertriglyceridemia, hyperproteinemia, hyperglycemia (add 1.6meq/L per 100mg/dL glucose) * Hypovolemic * Hypervolemic * Euvolemic

Answer 32

Order urine and serum sodium and osmolality

Answer 33

* Step one: mearure serum (plasma osmolaliry)-> If true (hypotonic, low osmolality), go to step two * Step two: Assess volum status if hypotonic/decreased osmolality to asses if hypovolemic cs euvolemic vs hypervolemic. If hypovolemic, go to step 3 * Step 3: Urine doium concentration. Urine sodium under 10 indicates extrarenal losss of volume (GI, blood or third spacing volume loss) with preserved renal ability to hold onto sodium (water and electrolyre conservation. Urine sodium over 20mmol suggests renal loss of volume (diuretics, vomiting, cortisol deficiency and salt wasting nephropathies

Answer 34

* Low: primary polydipsia or reset osmostat * High: SIADH

Answer 35

* DO NOT RAISE SODIUM LEVEL MORE THAN 6-12 meq/L in the first 24 hours-> Can cause Central Pontine Myelinosis * ALWAYS TREAT UNDERLYING DISORDER (IF KNOWN)

Answer 36

* **Hypovolemic**- Normal saline 500-1000mL/hr until BP stable, then 200mL/hr while checking sodium frequently to ensure only rising about 0.5meq/hr * **Hypervolemic**- Fluid restriction, treat underlying cause. In special cases: may use albumin, paracentesis; hemodialysis is definitive * **Euvolemic**- NS (small bolus) & Free water restriction. Caution: in SIADH, saline may worsen due to retaining the free water. No free water intake * **In emergency situations/severe hyponatremia with neuro deficits -> hypertonic saline 3% may be used in 100mL bolus**

Answer 37

* Syndrome of inappropriate antidiuretic hormone secretion (SIADH)-body makes too much antidiuretic hormone (ADH) – opposite to diabetes insipidus * ADH-helps the kidneys control the amount of water the body loses through the urine * Produced in the hypothalamus, released by the pituitary gland

Answer 38

* The plasma sodium concentration (PNa) is a function of the ratio of the body's content of exchangeable sodium and potassium (NaE and KE) and total body water (TBW) as described by Edelman's classic equation: * PNa ≈ (NaE + KE)/Total body water

Answer 39

* Antidiuretic hormone (ADH, arginine vasopressin) secretion results in a concentrated urine and therefore a reduced urine volume. The higher the plasma ADH, the more concentrated the urine. In most patients with SIADH, ingestion of water does not adequately suppress ADH, and the urine remains concentrated. This leads to water retention, which increases TBW. This increase in TBW lowers the plasma sodium concentration by dilution. * In addition, the increase in TBW transiently expands the extracellular fluid volume and thereby triggers increased urinary sodium excretion, which both returns the extracellular fluid volume toward normal and further lowers the plasma sodium concentration.

Answer 40

* Hyponatremia can occur in SIADH even if the only fluid given is isotonic saline. * In SIADH, the urine sodium concentration is usually above 40 mEq/L, the serum potassium concentration is normal, there is no acid-base disturbance, and the serum uric acid concentration is frequently low

Answer 41

* Treat underlying cause (hypothyroidism/adrenal insufficiency or infection) * Fluid restriction (~800ml/day) * Oral salt tablets * IV NS is frequently used in clinical practice, but may cause worsening hyponatremia * Hypertonic saline (if severe, aka seizures)

Answer 42

Vasopressin receptor antagonists * Conivaptan (IV in hospitalized) * Tolvaptan (oral in outpatient) * Produce a selective water diuresis without affecting sodium and potassium excretion

Answer 43

* Renal loss via diuretics, ACEI, ARBs, Hypoaldosteronism * Extrarenal loss – bleeding, pancreatitis, burns, GI loss * Clinical – dry mucous membranes, poor turgor, flat neck veins, hypotension, elevated hematocrit and serum protein, increased BUN: creatinine ratio (>20:1) (i.e. prerenal azotemia)

Answer 44

TX – you manage all of this with Normal Saline to correct the volume * Until which point will your Na raise with NS in the setting of hyponatremia

Answer 45

* High – Causes – Nephrosis, CHF * Clinical – EDEMA – peripheral and presacral, pulmonary edema, jugular venous distention, HTN, decreased hematocrit, decreased serum protein, decreased BUN: creatinine ratio * TX – treat acute/chronic renal failure, restrict H2O and salt

Answer 46

* Loop diuretics inhibit Na+, K+, Cl-, transport and Ca+ and Mg+ absorption. ADVERSE effect – decreased electrolytes "drain everything" * Thiazide diuretics – decrease urinary calcium excretion & Most likely among diuretics to cause hyponatremia. ADVERSE effects – decreases kidney’s ability to produce dilute urine, causes hypokalemia, hypomagnesemia, hypochloremia. "drain everything bur calcium'' * Potassium sparing diuretics (Triamterene/Spironolactone/Eplerenone/ACEI/ARBs) – ADVERSE effect - hyperkalemia

Answer 47

* Definition – serum potassium level less than 3.5 mEq/L * Results from insufficient dietary potassium intake, intracellular shifting of K+ from extracellular space, extrarenal potassium loss, or renal potassium loss. * Most common etiology – GI loss in diarrheal/Vomiting disease

Answer 48

* May produce non-specific symptoms- palpitations, weakness, fatigue, depression, myalgias * Associated with low magnesium levels * **Hypokalemia + Acidosis – profound K+ depletion and requires urgent treatment**

Answer 49

* Fatigue * Malaise * Muscle cramps * Muscle weakness * Constipation

Answer 50

* Severe cases; hyporeflexia, paralysis, hypercapnia, tetany and rhabdomyolysis * Hypertension may be present due to aldosterone or mineralocorticoid excess * Renal manifestations include nephrogenic KI and interstitial nephritis ## Footnote Hypokalemia assfectsmyscle contraction and cardiac conduction but does not cause seizures

Answer 51

K+ is low as a result of diarrhea, vomiting and inappropriately high with renal loss ECG – may show decreased amplitude, broadening of T waves (earliest sign), prominent U waves, premature ventricular contractions, and depressed ST segments.

Answer 52

**Oral potassium is safest route** – typically K-dur * Can administer 2 doses of 40mEq PO 1hr apart May give K+ IV for severe deficiency (slow infusion, ~20mEq/hr) Also correct Magnesium

Answer 53

* Flat T waves * U waves are present * Torades at the end * All of these point to low K+

Answer 54

* Definition – serum potassium greater than 5.0 mEq/L (in some laboratories 5.2) * 90% of potassium is secreted through the kidney * 98% intracellular while only 2% circulates in the blood * Most common cause is hemolysis, most common “real cause” is renal failure

Answer 55

* Stabilize the cardiac membrane * Shift potassium into cells * Remove potassium from the body

Answer 56

*MURDER Muscle weakness, Urine production, Respirataory failure, decreased cardiac contractility, Early muscle twiching and cramps, Rythm changes * Impairs neuromuscular transmission – causes muscle weakness (progressive ascending), flaccid paralysis and ileus (paralyzes intestinal muscles) * Do NOT rely upon ECG to catch hyperkalemia, but changes include **bradycardia, PR interval prolongation, peaked T waves, QRS widening and biphasic QRS-T complexes. BBB and AV block may occur.** * V fib and cardiac arrest are terminal events

Answer 57

Bradycardia, wide QRS, P wave flat * Hyperkal

Answer 58

* ACE inhibitors, ARBs and spironolactone, potassium-sparing diuretics should be used cautiously in patients with heart and/or liver failure and kidney disease * Repeat labs, check plasma potassium * Check renal panel – rule out kidney dysfunction

Answer 59

* Treatment emergent in patients with cardiac hx. * Hold exogenous potassium * Refer if hyperkalemia from kidney disease and with renal potassium excretion - nephrologist

Answer 60

* Normal – Total 8.5 – 10.5 mg/dL, Ionized 4.6 – 5.3 mg/dL * Necessary for muscle and nerve function * The calcium-sensing receptor, is a transmembrane protein and is located in the parathyroid gland and kidneys. * Functional defects in this receptor are associated with diseases of abnormal calcium metabolism

Answer 61

* The most common causes are advanced Chronic Kidney Disease due to decreased production of active vitamin D3, low albumin, hypoparathyroidism * Decreased intake or absorption * Increased loss * Endocrine disease

Answer 62

* Increases excitation of nerve, muscle cells (because decrease excitation threhold) – spasm, cramps, **tetany**, laryngospasm with stridor, seizure, paresthesia, pain * Classic sign – “Chvostek Sign” : The increased irritability of the facial nerve, manifested by twitching of the ipsilateral facial muscles on percussion over the branches of the facial nerve * Classic sign – “Trousseau Sign”: inflation os BP cuff above systolic BP for 3 mins causes painful carpal spasms->carpopedal latent tetany ## Footnote * CRAMPS: Confusion, Reflexes hyperative, Arrythmia (prolonged QT interval), Muscle spasms, Positive Trousseaus, Signs of Chvostek

Answer 63

* Tetany, arrhythmias, or seizures * IV calcium gluconate, continuous infusion

Answer 64

* Oral calcium – 1-2 g and Vit D. * Typically, calcium carbonate * Check urinary excretion of calcium – too high and it impacts renal function * **low Ca associated with hypoalbuminemia does not requires replacement**

Answer 65

* 90% - primary hyperparathyroidism and malignancy * Must look at duration and for a neoplasm * May affect kidney, GI and neuro function

Answer 66

Weakness, loss of reflexes, fatigue, constipation, polyuria, nausea, vomiting, anorexia, renal colic, nephrolithiasis * Pance: Nephrolithiasis, **bones**-bone pain, fractures, abominal **groans**-ileus, constipation. Decreased DTR and weekness, **psychic moans** (depression, anxiety, vognitive dysfunction) and increased vascular tone (HTN)

Answer 67

* Lab – ionized calcium exceeds 1.32 mmol/L * Remember- adjust calcium by adding /subtracting 0.08mg/dL for every 1.0 g/L albumin above or below 4 g/L * Severe: Think malignancy * ECG – shortened QT interval * CXR – granulomatous disease or malignancy

Answer 68

* Identify cause and treat cause * IVF’s to increase hydration to increase calciuresis * Don’t use thiazide diuretics to assist – may worsen * **Bisphosphonates** are treatment of choice for hypercalcemia of malignancy (may take up to 72 hours to reach full effect)

Answer 69

* Dialysis with low calcium dialysate may be needed. * Refer based on etiology * Symptomatic or severe hypercalcemia require immediate treatment * Suspected malignancy may require urgent, expediated evaluat

Answer 70

Calciphylaxis, also known as calcific uremic arteriolopathy (CUA), is a serious and rare condition typically seen in patients with end-stage renal disease (ESRD) on dialysis, but it can also occur in patients with normal kidney function. It is characterized by the calcification of small and medium-sized blood vessels, leading to blood flow obstruction, tissue ischemia, and necrosis. Here are some key points about calciphylaxis:

Answer 71

* Plasma phosphorus represents a small fraction of total body phosphate (2%) * Primary determinants – renal excretion, intestinal absorption, shift between intracellular and extracellular spaces. * Kidney is the most important regulator

Answer 72

* Renal proximal tubular reabsorption of phosphate is decreased by volume expansion, corticosteroids and proximal tubular dysfunction. * Growth hormone increased proximal tubular reabsorption. * Intimately related to calcium metabolism

Answer 73

Hyperphosphatemia – most common cause is ESRD – tx with phosphate binders, calcium acetate, calcium carbonate, or Sevelamer, hydrate * Clinical manifestations: Usually due to low calcium (tetany, prolonged QT on EKG) * If calcium not low pathological calcifications * Treated with low phosphorus diet, saline infusion/loop diuretics, calcium acetate (PhosLo), dialysis

Answer 74

Hypophosphatemia – Vitamin D deficiency, respiratory alkalosis (shifts PO4 intracellularly), excessive IV glucose, decreased GI absorption – tx with phosphate repletion * Alcoholism = MCC * Clinical manifestations: weakness, CHF, respiratory failure (all muscles need PO4 to function), seizures, coma, AMS * Treated with oral phosphorus and/or IV (sodium phosphate or potassium phosphate)

Answer 75

* Normal plasma magnesium concentration is 1.8 – 3.0mg/dL * One third bound to protein and two-thirds existing as free cation. * Excreted through kidney * Physiologic effects on the nervous system mimic those of calcium.

Answer 76

* Mag and Calcium are best friends (and coexists with K) – if one is not right, more than likely the other will not be right. * Remember – serum Mag may be normal in mag depletions – check urine mag

Answer 77

* Shares many etiologies with hypokalemia * Renal potassium wasting also occurs from hypomagnesemia * Potassium replacement will not work until you correct the hypomagnesemia.

Answer 78

* weakness, cramps, neuromuscular and central nervous system hyperirritability, tremors, nystagmus, Babinski, HTN, Tachycardia and ventricular arrhythmias. * Lab – urinary excretion of magnesium exceeding 10-30 mg/day, hypocalcemia and hypokalemia are often present. * ECG may show prolonged QT interval, pTH secretion is often suppressed.

Answer 79

IV Magnesium Sulfate (over 1-2hr; if infused over 15 mins – acts a soft tissue muscle relaxant)

Answer 80

* Often associated with advanced CKD and impaired magnesium excretion or chronic intake of mag containing drugs. * Folks forget antacids and laxatives are sources of mag. * IV Mag used for preeclampsia and eclampsia * Very easy to induce hypermagnesemia when attempting to replace in CKD

Answer 81

* Stop any source of Mag * Calcium antagonizes – give calcium chloride 500mg or more at rate of 100mg per minute. * May need Hemodialysis or peritoneal dialysis to remove mag – especially in severe CKD

Answer 82

* In practice, this is estimated through prediction equations for GFR based on serum creatinine using age, gender, and ethnicity * Reflects the ability of the kidneys to filter fluids and various substances, including medications.

Answer 83

* Normal findings 10-20mg/dL (slightly higher in elderly, slightly lower in children) * **Critical value >100mg/dL** * Rough measurement of renal function/GFR * Urea is formed by liver and therefore is also measurement of liver function

Answer 84

* Interpreted in conjunction with creatinine- ie BUN/creatinine ratio * Many causes of elevation including dehydration, shock, burns, CHF, GI bleeding, ureteral obstruction, primary renal disease, nephrotoxic drugs

Answer 85

* Normal findings- 0.5-1.2 mg/dL (varies by gender and age) * **Critical value >4mg/dL** * Catabolic product of creatine phosphate * Unlike BUN, aside from dehydration, only renal disorders and urinary obstruction will cause elevation in creatinine

Answer 86

* There is some fluctuation with muscle mass, protein consumption, age * Used to estimate glomerular filtration rate (GFR)

Answer 87

* Collect it midstream or by cath * First morning specimen: urine is more concentrated & contains higher levels of cellular elements & other components * Suprapubic aspiration is gold-standard in Dx of UTI <2yo (rarely done)

Answer 88

* Dipstick within 30-60mins of collection followed by microscopy if dipstick has positives * Microscopy – centrifuged urinary sediment – looking for crystals, cells, casts and infectious organisms * A normal sediment (made of Tamm-Horsfall proteins) is termed “bland”

Answer 89

* Normal: clear * Color: Straw Yellow * Bright yellow – B2 * Orange – Pyridium * Purple – UTI * Red – food coloring * Brown – Bile or AGN

Answer 90

* DKA- sweet smell of acetone * Fecal odor- enterovesical fistula * Foul odor- UTI * Ammonia odor – prolonged retention within bladder (BOO/underactivity)

Answer 91

* Normal urine volume is 750 to 2000 ml/24hr * Varies with state of hydration, metabolic state, hormonal influence

Answer 92

* Polyuria: DM, DI, Diuretic use, Psychogenic * Oliguria (<30cc/hr): Pre-renal vs. Renal vs. Post-renal causes

Answer 93

* Normal: 0-8 mg/dL; Proteinuria = 150mg/24hrs; Nephrosis = >3.5g/24hrs * Normally not present because the glomerular membrane openings are too small to allow them to pass through * Dipstick is sensitive to albumin; may miss small concentrations of γ-globulins and Bence Jones proteins * **Sulfosalicylic acid test** method is a more sensitive precipitation test. It can detect albumin, globulins, and Bence-Jones protein at low concentrations.

Answer 94

* Proteinuria is a common and important indicator of renal disease * Tamm-Horsfall Protein is exclusively produced by renal tubular cells of the distal loop of Henle and is the most abundant normal urinary protein * Follow-up testing may include 24-hour urine protein measurement and urine protein/creatinine ratio

Answer 95

* Normal: none, because it is always reabsorbed by proximal tubule * Elevated in hyperglycemia or glomerulus damage * Glycosuria occurs when filtered load of glucose exceeds ability of tubule to reabsorb it (180- 200 mg per dL) i.e. “renal threshold” * Etiologies include DM, Cushing's syndrome, liver pancreatic disease, & Fanconi's syndrome (tubular waste disease).

Answer 96

* Normal: 1.010-1.030 (some sources say 1.005-1.030) * Measure of concentration of waste and electrolytes in the urine * High = concentrated urine, Low = dilute urine * Always in comparison to distilled water

Answer 97

* Evaluates concentrating power of kidney * Overhydration becomes dilute while dehydration becomes concentrated * Any high-density radiopaque dyes, high glucose or any contamination with have SG >1.035

Answer 98

* Normal: none * Screen to detect leukocytes present in the urine * 90% accurate in predicting WBCs in the urine

Answer 99

Normal: none Generally, Ketones consist of beta-hydroxybutyric acid (78%), acetoacetic acid (20%), and acetone (2%) * Indicates that insulin is lacking and fatty tissue is being metabolized * Only acetoacetic acid is detected on UA dipstick * Only beta-hydroxybutyric acid is specific for DKA

Answer 100

* Indicates hyperglycemia/ poorly controlled DM (typically type 1) * In absence of glycosuria, ketone bodies suggest starvation * Can also be elevated in other diseases of ketosis: alcoholism, fasting/starvation/dehydration, isopropanol ingestion * Occasionally seen in febrile illnesses in children

Answer 101

* Normal: none * Conjugated with glucuronic acid (direct) bilirubin can be excreted into the urine after conversion to urobilinogen in intestines and reabsorbed * Unconjugated or indirect is bound to albumin, and is therefore not water soluble and cannot be excreted in the urine

Answer 102

* Elevation indicates disease of bilirubin metabolism after conjugation * Urobilinogen indicates overproduction of bilirubin * Less important marker of liver disease than serum levels

Answer 103

* Normal: none but are commonly seen * Uric acid crystals: think gout * Phosphate and calcium oxalate crystals: think parathyroid abnormalities, malabsorption * Concern with crystals is formation of stones

Answer 104

Casts form when urine flow is slow or glomerulus is inflamed * WBC/RBC casts only form in DCT and CD * Tamm-Horsfall protein and albumin act like glue for casts If there are many red or white blood cells in urine, cellular casts form.

Answer 105

* Pigmented granular casts (called Muddy Brown casts) + renal tubular epithelial cells alone or in casts are hallmarks of acute tubular necrosis * White blood cells + white blood cell casts + proteinuria can be seen with pyelonephritis and interstitial nephritis. * Protein + hematuria with acanthocytes + red blood cells casts – highly suggestive of glomerulonephritis

Answer 106

* Clinically significant if there are more than three red cells per high-power field on at least two occasions. * No casts? = Distal to kidney bleed * False positives on dipstick – myoglobin, oxidizing agents, beets, rhubarb, hydrochloric acid, bacteria, factitious.

Answer 107

* Transient hematuria is common and less often a concern in younger population due to lower concern for malignancy * Exercise-induced hematuria is a relatively common, benign condition often associated with long-distance running. Repeat urinalysis 48-72 hour later should be negative.