nephrology chronic renal failure

7/30/2019 Nephrology Chronic Renal Failure

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CKD/CRF

-DEFN:o *CKD is defined as EITHER:

kidney damage decreased function (decreased GFR) for 3 or

more months

-kidney disease can be dx w/out knowledgeof its cause

-kidney damage is usually ascertained byMARKERS:

o -rather than by kidney biopsy -MARKERS of kidney damage:

o *PROTEINURIA- -persistent proteinuria is

the PRINCIPAL MARKER of

kidney damage

-an albumin/creatinineRATIO greater than 30mg/g in SPOT urine

samples is usually:

*consideredABNORMAL

o *other markers include: -urine sediment -abnormalities in BLOOD

and URINE chemistry

-abnormal findings onimaging studies

o *persons w/: -normal GFR- BUT w/

MARKERS of kidney

damage are:

*at INCREASEDRISK for adverse

outcomes of CKD

-CRF implies: *PERMANENT damage to the kidney -the normal architecture is gradually

REPLACED by SCAR TISSUE

-the HALLMARK of RENAL FAILURE is: *ELEVATION of the CREATININE and BUN

concs in the extra-cellular fluid caused by: -a FALL in the GFR *other fns of the kidney are also impaired,

such as:

-SYNTHESIS of renal HORMONES *a wide range of sxs accompany the various

degrees of renal failure

-several TERMS are used to describe chronicrenal injury:

*CRF:-is the general term used to describe

IRREVERSIBLE loss of GFR over a prolonged

period of time- usually YEARS

*CHRONIC RENAL INSUFFICIENCY:

-implies MILD CRF

*AZOTEMIA:-refers to an ELEVATION in the BUN and

CREATININE levels, and DOES NOT

imply:*any sxs OR overt clinical

manifestations of kidney disease

-azotemia occurs w/ BOTH chronic and

acute renal failure

*UREMIA:-is the SYMPTOMATIC phase of renal failure

during which:

*sxs and signs of renal dysfn are DETECTED

-for many individuals- uremicmanifestations do NOT appear UNTIL:

*the GFR is LESS than 10 ml/min (normal

120 ml/min)

*END-STAGE RENAL DISEASE (ESRD):-refers to any form of CHRONIC (ie-

IRREVERSIBLE) renal failure at a stage that:

*PERMANENT renal replacement therapy is

indicated in the form of:-dialysis/transplant

*NORMAL renal architecture is LOST and:-REPLACED w/ COLLAGEN

-as this occurs:

*the SIZE of the KIDNEYS generallyDECREASES

* HYPER-FILTRATION HYPOTHESIS:

***a popular explanation for the PROGRESSIVE

NATURE of CRF is termed:

-the HYPER-FILTRATION HYPOTHESIS:

*this hypothesis states that- the INTACT nephrons

are EVENTUALLY INJURED by:

-the increased plasma flow AND hydrostatic pressure

*healthy remnant nephrons sustain damage as a

result of:

-LONG-TERM exposure to:

*INCREASED capillary PRESSURE and FLOW

*hyper-filtration injury leads to a CHARACTERISTIC

glomerular injury pattern known as:


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-FOCAL GLOMERULAR SCLEROSIS

*this hypothesis explains why renal failure

CONTINUES to progress even when:

-the initial renal insult is self-limited

*eg- some forms of glomerulonephritis

*HYPER-FILTRATION INJURY can be DIMINISHED by:

-REDUCING glomerular HYDROSTATIC PRESSURE

-several methods of lowering glomerular pressure

have been tried in an attempt to:

*slow or halt the progression of CRF

(low protein diet (= hyperfiltraxn

injury)= RBFand Pgc

*INCREASED SNGFR (ie- HYPER-filtration) occurs by:

-

DILATATION of AFFERENT glomerular arterioles,

resulting in:enhanced single-nephron PLASMA FLOW

-

filtration may also be enhanced by:

*INCREASED EFFERENT arteriolar TONE

CRF CLINICAL SX-GFR


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Specific CRF Sx details

-*SODIUM RETENTION (Na excrexn) results in:

-EXPANSION of the extra-cellular space, which is

manifest as:

1. EDEMA 2. HYPER-TENSION

require: a sodium-RESTRICTED DIET

*HYPERKALEMIA restrict K+ intake

-(arrhythmias/Gut K+ secrexn)

*ACID-BASE: METABOLIC ACIDOSIS

(RETAIN ammonia) bone buffers w/Ca rel-> bone

Dx)

(retain P -> anion gap acidosis)

*BONE DISEASE: RENAL OSTEODYSTROPHY

*RENAL OSTEODYSTROPHY summary:

___________________________________________

DECREASED vitamin D

HYPO-calcemia

AND

DECREASED excretion of PO4-

HYPER-phosphatemia

___________________________________________

DECREASED vitamin D

AND

HYPER PTH

(osteitis fibrosa cystica/osteomalacia-antacid)

HYPO-calcemia

___________________________________________

Secretion of PTH

RENAL OSTEODYSTROPHY

*CHANGE DRUG DOSAGE IN CRF PTS:

-its necessary to:

*REDUCE the DOSE -or- EXTEND the dosing

INTERVAL of drugs that are:

-EXCRETED by the KIDNEYS

-drugs that are REMOVED by the KIDNEYS include:

*aminoglycosides/vancomycin/PCN/allopurinol/digo

-in CONTRAST- LIVER drugs dont req adjustment:

*erythromycin/phenytoin/anticoags/narcotics

*CNS

(uremic toxin accumulation leads to lower seizure

threshold)

-Asterixis: involuntary hand jerking -> seizures

-subtle ECG changes

-peripheral sensory neuropathy

*CARDIOVASC

-dyslipidemia/-stroke

-the ability to ELIMINATE a SALT LOAD may becomeCOMPROMISED is some pts w/ CRF, leading to:

*EXPANSION of the extra-cellular VOLUME

-EDEMA formation: CHF + pulm edema

-w/ ADVANCED renal failure- pts may develop an:

*ACUTE PERICARDITIS (infl./hemmor): (uremic

toxins in pericardial space)

-Sx: chest pain/SOB/pericardial frixn

rub/TAMPONADE (hypoTN)

*METABOLIC/ENDOCRINE:

*glucose intolerance AND insulin resistance*hyper-

lipidemia/DECREASED levels of testosterone AND

estrogen (fertility)


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ACUTE RENAL FAILURE

GFR/

Cr+BUN (cuz urea reab=prerenal-low flow)

(Cuz Cr secreted so Cr= UT

obstruxn/hydronephrosis)

SAME-ratio can be same if both Cr/BUN inc

*ARF DEFIXN

--acute renal failure is a common clinical syndrome

-its DEFINED as:

*increase of 0.5 mg/dL from baseline occuring over

days (< 1 month) of:

-the BUN or CREATININE

*OR- 50% DECLINE in calculated GFR

*its easy to miss the early changes

-the clinical manifestations of this d/o arise from the:

*DECLINE in GFR

*and the INABILITY of the KIDNEY to

EXCRETE toxic wastes produced by the body

-its recognized clinically by:

*RISING levels of BUN and CREATININE

*and usually a REDUCED URINE OUTPUT

-most forms are REVERSIBLE processes

-most physicians accept the definition of acute renal

failure as a:

*RISE in plasma CREATININE of 0.5 mg/day

*and- a RISE in BUN of 10 mg/dl/day

*over several days

*THREE CAUSES OF ARF:

1. PRE-RENAL

*ie- functional

*generalized or local

*DECREASE in RBF and/or Pgc

(-> GFR + Cr +BUN)

-BUN/Cr = 20:1

*occurs BEFORE the GLOMERULUS

(Esp if have: poor tissue perfusion= hypoTN/

dehydraxn/hemorrhage/edema due to CHF or

nephrotic or cirrhosis)

2. INTRA-RENAL

*ie- structural

*intrinsic renal disease leading to:

-DAMAGED NEPHRONS

-KIDNEYS ENLARGED

3. POST-RENAL

*ie- obstructive

*obstruction in the urinary tract

(crystals/BPH)

*occurs DISTAL to the cd

(Dx: oliguria -> anuria -> BUN/Cr is over 20:1

Suprapubic//flank pain

Urinalysis: hematuria +uric acid crystals (urea/Cr

ratio > 1) or normal (if BPH)


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*DIAGNOSIS OF PRERENAL AZOTEMIA:

*DIAGNOSIS:

-in pts w/ VOLUME DEPLETION/DEHYDRATION:

* history of vomiting diarrhea, or diuretic use

*physical exam may reveal:

-poor skin turgor

-orthostatic hypo-tension

-tachycardia

-conversely- pts w/ RELATIVE DECLINES in

EFFECTIVE ARTERIAL BV from:

*CHF , nephrotic syndrome, or cirrhosis

*may show:

-peripheral edema OR ascites

-

URINALYSIS UNREMARKABLE, except for

-increased # of hyaline and granular casts + less Na

(Cuz kidney NOT intrinsically diseased)

-Response to poor perfusion in ARF:

-Na reab (SNS/aldo) (=less Na in urine)

- H20 reab (ADH)

-BUN/Cr = 20:1 (cuz -Na reab -> coupled urea

reab -> BUN) PRERENAL AZOTEMIA

*DIAGNOSIS OF POSTRENAL AZOTEMIA:

-OBSTRUCTIVE (DISTAL TO CD)revible

(Causes: intrarenal crystals, renal pelvis or ureter

caliculi, or BPH or neoplasia/ chemoTx leads to acute

urea nephropathy ( lysed cells -> urea -> uric

acid crystals -> ARF!)

-Dx: oliguria -> anuria -> BUN/Cr is over 20:1

Suprapubic//flank pain

Urinalysis: hematuria +uric acid crystals (urea/Cr

ratio > 1) or normal (if BPH)

IMAGING:

* DX of obstruction depends on radiography:

Ultrasonography

-IVP (b/c of the decline in renal fn- the IVP vis

ualization of the collecting system in obstruction

may not occur until 6-24 hrs after dye administration

-CT scanning

-or- retrograde pyelography

*DIAGNOSIS OF INTRARENAL ARF (#1):

--BUN/Creatinine BOTH RISE and:

*ratio NORMALIZES

-urinalysis becomes ABNORMAL

-tubular fn DIMINISHES

-signs of UREMIA develop

-Causes: ATN (85%)/ AIN (allergy/eosinos)/Acute

GN (RPGN)

-Intrarenal SX:

-GFR (intrarenal vasoconstrixn -> RPF + O2

to outer medulla/PST/TAL

-Segmental patches of NECROTIC lesions

-URINALYSIS: Casts:

-made up ofCELLULAR DEBRIS from injured or

necrotic renal tubule cells are freq found in the

DISTAL NEPHRON, where they:

*IMPEDE the FLOW of URINE

*the necrotic cells SHED into the tubular LUMEN:

-> REDUCE renal EXCRETORY FN:


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*not only by- OBSTRUCTING urine flow

BUT -BACK-LEAK OF GLOMERULAR FILTRAXN=leave

gaps along the tubular epithelia thru which

glomerular filtrate can RE-ENTER the circulation, a

process called: BACK-LEAK OF GLOMERULARFILTRATE

TYPES OF INTRARENAL ARF:

*ATN

-ISCHEMIC (#1) (HYPOTXN -> STRUCL DAMAGE) OR

TOXIC

-*CAUSES of ischemic insult include:

-hemorrhage

-hypo-tension (cardiac sepsis)

-often occurs in the presence of:

*NSAIDs, and ACE inhibitors

-these are ALL the causes that give rise to:

*PRE-RENAL AZOTEMIA (high ratio, but tubules look

normal)*BUT- the nephron cannot tolerate this state

long SO:

-condition EVOLVES from pre-renal to: INTRARENAL

*CAUSES OF TOXIC ATN:

1. Antibiotics

Aminoglycoside/ amphotericin B/cyclosporine:

(used to prevent graft -vs- host disease in

transplants)

2. Heavy Metals

-cis-platin- dose-dependent

-salts of mercury, arsenic, bismuth, silver, chromium

3. Radio-contrast Agents

-this form of nephrotoxic ATN can present

w/ an FENa o fLESS than 1%

-CT Scans and angiograms deliver the most toxic

dyes to pt

4. Endo-geneous Toxins

-

myoglobin, hemoglobin, and myeloma light chains

TOXIC SX: kidneys ENLARGED (PCT)

-MICROSCOPIC: *focal (patchy lesions)

*proximal tubule NECROSIS and APOPTOSIS

*DISTAL CASTS: -hyaline-and- PIGMENTED -

HALLMARK of ATN

*sloughed tubular epithelial cells

-they're RBCs (pigmented)

ISCHEMIC SX

-EOSINOPHILIC HYALINE CASTS as well as

PIGMENTED GRANULAR CASTS are common, esp in

the: *distal tubules and- collecting ducts

-these CASTS consist of:*TAMM-HALL PROTEIN

-a specific urinary glycoprotein normally secreted by

the cells of ascending thick limb and distal tubules

*in conjunction w/ Hb/Mg.

-other findings in ischemic ATN are:

*interstitial edema

*and- accumulations of leukocytes w/in dilated

vasa recta


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*LABORATORY TESTS:

-the URINE SEDIMENT in the EARLY phase of ATN

usually contains:

*renal tubular epithelial cells/ granular and

epithelial cell casts

-b/c TUBULAR FN is IMPAIRED:

*the kidney's ability to conserve Na and maximally

concentratethe urine is diminished

-in pts whose AZOTEMIA is SECONDARY to PRE-

RENAL CAUSES:

*the urinary indices usually show:

-urinary osmolality GREATER than 500 mOsm/kg

water

-urinary Na conc LESS than 10 mEg/L

-urine-plasma creatinine ration LESS than 20

-these ranges are diagnostic in ~80% of cases

**FE NA

*FENa is GREATER than 1% in pt's w/:-ATN

*FENa is LESS than 1% in pts w/:-PRE-RENAL

AZOTEMIA

*pts w/ radiocontrast induced acute renal failure

often have: -FENa values LESS than 1% though ATN is

PRESENT

*


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nephrology chronic renal failure

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