Pete A. Gutierrez MD, MMS, PA-CMiami Dade College

Physician Assistant Program March 2009

NephrologyUrine Analysis:

Dip stick testing: Problems:

Urine Ph may change with time Contamination may cause bacteria to multiply and

convert nitrate to nitrite causing a false positive. At low specific gravity (Less than 1.010), cells lyse

and casts from less readily. Cast also dissolve in alkaline Urine.

NephrologyMidstream Urine Collection

Contamination more common in women than in men.

Suprapubic aspiration is the more secure method of getting an Uncontaminated Urine

Hematuria Flank Microscopic

NephrologyUrine Casts.Urine Casts. Are formed from Tamm-

Horsfall glycoprotein which is synthesized and secreted in the ascending limb of the loop of Henle and distal convoluted tubules.

Physiologic Casts Hyaline are transparent and cylindrical and are seen in urine of normal subjects.

Both can be increased by fever, exercise and volume depletion

NephrologyPathologic casts: this may contain cellular

material (erythrocytes, leukocytes, tubular cells, bacteria, or fungi) , fibrin, lipids, bile, and crystals.

The most important is the erythrocytes, because it indicates glomerular bleeding.

Those composed of polymorphonuclear leukocytes usually indicate renal parenchyma infection.

NephrologyLeukocytes in the urine means infectionRenal tubular cells are found in the urine

in acute tubular necrosis and acute interstitial nephritis

Crystals of calcium oxalate and uric acid may be seen in normal urine however large bizarre crystals of any type including calcium oxalate and uric acid indicate calculus disease.

NephrologyIGA nephropathy:

The most common form of primary glomerular disease in the world.

It is particular prevalent in Asia, and Australia, and rare in African Americans.

It originally thought to be benign.Now understood it will progress to renal

failure in 20 to 40% of patients affected.

NephrologyPrimary gross hematuria, No therapeutic regimen has been shown to

clearly affect the outcome in IgA disease.However warfarin and dipyridamole with or

without cyclophosphamide have been suggested as worthy of further investigation

Also omega 3 fatty acids, ACE, and long term steroids are also on trial.

NephrologyMembranous nephropathy:

Two thirds of patients with this disorder either have a spontaneous remission or have stable or very slow progressive renal insufficiency.

Those with heavy proteinuria greater than 10 gram per day, hypertension, diminished GFR, male gender, don’t do well.

NephrologyBacteria:

Gram Negative E-Coli Klesbsiella Pneumoniae Proteus Enterobacter Pseudomonas

NephrologyGram Positive

Staphylococcus saprophyticusStaphylococcus aureusStaphylococcus not aureusEnterococciOther bacteria mixed Yeast

NephrologySymptomatic UTI’s:

Obstruction to urine flow. Congenital anomalies Renal Calculi Ureteral occlusion (partial or total). Vesicoureteral reflux Residual urine in bladder Neurogenic bladder Urethral stricture Prostatic hypertrophy

NephrologyInstrumentation of urinary tract;Indwelling urinary catheterCatheterizationUrethral dilationcystoscopy

NephrologyAcute Urethral syndrome:

Vaginitis approximately 20% of women in the United States have an episode of dysuria each year. (Candida is the most common cause).

Urethritis most commonly cause by Chlamydia trachomatis

Prostatitis The most common addiction in men causes dysuria and urinary frequency. (E. Coli).

NephrologyPregnancy and the increases risk of UTI:

20-40% of which develop pyelonephritis.Either short acting sulfonamides or amoxicillin

for 7 days usually suffices.Avoid Tetracycline, trimethropin and

fluoroquinolones.

NephrologyHypertensive disorders of pregnancy:

Preeclampsia is characterized by, 1. Hypertension, proteinuria, edema, and at time coagulation and liver abnormalities usually occurring at about the (20) weeks of pregnancy. Primarily in nulliparas. Pressure of 140/90.

Patient will go into convulsions and diet condition called eclampsia.

NephrologyKidney function and morphology in

preeclampsia:Both GFR and RPF decrease in preeclampsia.Uric acid increases in blood.Increased proteinuria.Calcium develop hypocalciuria Lesion at the glomerular capillary

endotheliosis.

NephrologyManagement of preeclampsia:

Hospitalization rest and if signs of impeding eclampsia(hyperreflexia, headache, epigastric pain) develop termination of pregnancy should be considered.

The drug of choice for impeding convulsion is parenteral magnesium sulfate.

NephrologyRegulation of blood pressure:

Hydralazine administered intravenously is the drug of choice. (5mg as a bolus follow by 5-10mg every 20-30 minutes.

Labetalol intravenously 20mg and repeat the dose every 20 minutes, up to 200 mg.

Refrain from using nitroprusside.

NephrologyUse of Radiologic Techniques:

KUBIntravenous pyelography (IVP) Stone,

obstruction. (allergic reactions).Cystography (Bladder).UltrasoundCt evaluation of renal diseaseMRI

NephrologyRenal angiography provides definitive

diagnosis of renal arterial pathology

NephrologyAlgorithm for treatment of hypertension:

First line of therapy should be diuretic (thiazide).In patients with type I diabetes and proteinuria

(Diabetic nephropathy) the treatment is with an ACE inhibitor.

In patients with heart failure (Systolic dysfunction), ACE inhibitor or diuretic is indicated

Beta blockers or Ca Channels blocker can them be use.

NephrologyCauses of resistant Hypertension:

White coatPseudohypertension in elderly personsUse of improper size blood pressure cuff.Patient non compliantFailure due to cost, side effects, or ignoranceDietary noncomplianceExcess salts.

NephrologyCauses of resistant Hypertension:

Excess ethanol intakeVolume overloadFailure to include diureticInadequate treatmentMedication interactions.Nonsteroidal meds.Trycyclic antidepressantsCocaine or other illicit drugs

NephrologyCauses of resistant Hypertension:

Associated co morbid conditionsObstructive sleep apneaIncreasing obesityAnxiety induced hyperventilation or panic

attacks.

NephrologyCauses of resistant Hypertension:

Underlying secondary hypertension Reno vascular hypertension Primary renal parenchyma disease Primary Hyperaldosteronism Pheochromocytoma

NephrologyEvaluation of suspected renovascular

hypertension:The principal cause is atheromatous narrowing

of one or both main renal arteries, which occurs in older individuals, with a peak incidence in the sixth decade.

Men are affected twice as often as women.

NephrologyA second type of lesion is the fibro muscular

dysplasia (Hyperplasia) the lesion appears as a multifocal “string of beads,” beginning in the middle of the renal artery.

Test of choice is the renal angiography.Treatment must be aggressive.

NephrologyDiuretics:

LoopK-sparing OsmoticCarbonic anhydrase inhibitors

Nephrology Nephritis vs. Nephrotic:

In Nephritis syndrome there is variable proteinuria and active urine sediment; dysmorphic RBC’s and WBC’s and casts of RBC, WBC, and granular material. (Remember that CASTS always originate in the renal tubules).

Common causes of Nephritis syndrome are post infections GN, IgA Nephropathy, and Lupus Nephritis.

NephrologyNephrotic Syndrome:

Always heavy proteinuria, and urine fat.Nephrotic range proteinuria is >2.5-3.5gm/day.(Free fat droplets, oval fat bodies, fatty/waxy

casts and renal tubular cells with lipid droplets).Nephrotic patients tend to get hypoalbuminemia

(with 2nd edema) and they develop tendency for more infections, especially with H. Influenza, and S. Pneumonia.

Also low thyroid binding protein so low total thyroxine and iron levels.

NephrologyThe Nephrotic patient also have severe

hyperlipidemia.IgA Nephropathy most common >25%, also

know as Berger Disease.It can present from hematuria alone Berger

disease to Schonlein Henoch Purpura, which is found in children's, affecting the skin the kidneys and the joints.

The Hematuria is usually present secondary to an infection or exercise.

NephrologyMembranoproliferative AGN:This presentation has both basement membrane

and changes in cells proliferation.Presentation is similar to IgA with Hematuria with

nephrotic range proteinuria and rapidly progressive glomerulonephritis, and may lead to renal failure.

Rapidly Progressive AGN:Starts with azotemia, oliguria followed by diuresis in

days to weeks after which the GFR usually returns to normal. Rapid progression to renal failure

NephrologyDiabetic Nephropathy:

Is the second commonest cause of nephrotic range proteinuria.

In develops in 30% of the adult population with type I Diabetes.

First change in renal problems is micro albuminuria.

Patients progress to full renal failure within 5-7 years.

Need to control tight control of blood sugar level in order to prolong the disease process.

NephrologyAcute Intestitial diseases:

They present with slight proteinuria < 2mg/d.Acute allergic interstitial nephritis (AIN) is a

drug induced hypersensitivity problem and often presents with eosinophils.

The most common drug is cimetidine, thiazides, phenytoin, and allopurinol.

The most common antibiotics culprits are: Beta-Lactams like methicillin, TMP/SMX, and

Rimfapin, also fluoroquinolones.

NephrologyHereditary Kidney diseases:

Alport Syndrome= nephritis can be either X-linked or AD with variable expression, men are affected more than females.

Is a connective tissue defect(type IV collagen) which affect the basement membrane.

Target is the same as Goodpasture syndrome with occasional deafness and lens problems.

The female X l;inked had usually microscopic hematuria.

Males have renal failure before age 50.

NephrologyPolycystic kidney disease:

Autosomal dominant. Is the commonest genetic disease of the kidney. Usually associated with a mutation on the short arm of 16.

Patients develop cysts in the kidneys, liver and pancreas and associated with recurrent hematuria.

Progressive renal failure and HTN are the norm.Cerebral aneurism is a very small percent 1-5%.For kidneys infections use the lipid soluble

antibiotics like trimethroprim, erythromycin, chloramphenicol, tetracycline, ciprofloxin and clindamycin.

NephrologyDKA:

Occurs in 5% of patients with Type I DM. Laboratory shows increased ion gap. Metabolic acidosis,

and positive serum ketones in the urine., with plasma glucose usually elevated. Hyonatremia, hyperkalemia, azotemia, and hyperosmolality are other findings.

Clinical features: Nausea Vomiting And vaguely localized abdominal pain. Dehydration Respiratory shock Coma

NephrologyManagement:

ICUReplacement of fluids deficits of several liters.

(subtracting present weight with known recent weight).

At least one liter an hourInsulin therapyIV bolus of regular insulin at 10-15 units follow

by an infusion of 10-15 units/hour.A decrease of 50-75 mg/dl/hour is an

appropriate response.

NephrologyDKA continued:

When serum bicarbonate rises to 15 mEq/L 1-2 units/hour of insulin is the goal.

Start Dextrose %% should be infused once plasma glucose degreases to 250 mg/dl in order to prevent hypoglycemia.

Potassium deficits can be restore by adding 10-20 mEq/hour in the IV fluids.

Monitoring of blood glucose every 1-2 hours and arterial blood gases as often as necessary.

NephrologyComplications of DKA:

Lactic acidosisArterial thrombosisCerebral Edema