med 3.1 renal symptoms 1
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TRANSCRIBED BY: LUKE, LEIA, HAN, CHEWBACCA
Page 1 of 6
Alfredo Guzman, M.D.
Wag mong hanapin sa butas ng donut ang sarap Ron Capinding Paulo Coelho
Renal Symptoms
3.1 04 Nov
2014
REVIEW OF ANATOMY
GROSS ANATOMY
Bean-shaped Divided into 2 parts
o Cortex (outer portion); contains all the glomeruli o Medulla (inner portion)
*Tubules are located in both the cortex and the medulla
MICROSCOPIC ANATOMY
NEPHRON
o Basic unit of the kidney o Each nephron is composed of a tuft of capillaries called the
glomerulus Glomerulus lies between the 2 arterioles (efferent and afferent) After the glomerulus series of tubules , the length of which depends
on where the glomerulus is located
FUNCTIONS OF THE KIDNEY
1. Regulation of the composition and volume of body fluid (Obligate H2O loss = 500mL/day)
2. Aid in the control of systemic blood pressure 3. Bio-activation of vitamin D3
implication: Calcium Metabolism
o Vit D3 aids in calcium absorption D3 serum Ca level PTH Ca and PO4 Renal Osteodystrophy bone demineralization d/t
chronic renal disease
4. Regulation of red cell mass by erythropoietin production
o Renal Failure can lead to anemia d/t
erythropoietin
uremic toxins in RBC
CLINICAL MANIFESTATIONS OF RENAL DISEASES
1. Glomerular 2. Tubular 3. Interstitial 4. Vascular
FROM 2B 2016
Clinical manifestations of these disorders depends on the pathophysiology of the renal injury
Nephrologic syndromes usually consist of several elements that reflect the underlying pathologic processes
Duration and severity of the disease will affect these findings and typically include one or more of the following: o disturbances in urine volume (oliguria, anuria, polyuria) o abnormalities of urine sediment (RBCs, WBCs, casts, and
crystals) o abnormal excretion of serum proteins (proteinuria) o reduction in GFR (azotemia) o presence of hypertension and/or expanded total body fluid
volume (edema) o electrolyte abnormalities o in some syndromes, fever/pain
AZOTEMIA
elevation of water-soluble metabolites in blood
retention of nitrogenous waste products (creatinine, urea) d/t reduced GFR
results from: o reduced renal perfusion o intrinsic renal disease o postrenal processes (ureteral obstruction)
no associated symptoms
GFR
serum creatinine is the most widely used marker for GFR
directly proportional to urine creatinine excretion and inversely to serum creatinine (UCR/PCR)
Urea
not constant
reabsorbed by the tubule
Azotemia Uremia
Elevation of water soluble metabolites in the blood
Not associated with symptoms
Same as above but with associated symptoms
First Sx: Sleep disturbances
SERUM CREATINE
More reliable index of glomerular filtration rate (GFR) than urea because of the latter's lower back-diffusion from tubule lumen to peritubular blood
Mainly derived from metabolism of creatine or creatine phosphokinase from skeletal muscle cells
Produced in almost constant rate
Steady state concentration dependent on renal excretion w/c mainly reflects of GFR
APPROACH TO THE PATIENT: AZOTEMIA
decide if reduced GFR represents acute or chronic renal injury
clinical situation, history, and laboratory data helps in diagnosing
REDUCED SINGLE NEPHRON GLOMERULAR FILTRATION RATE
TUBULAR FUNCTION NORMAL
Tubular function is still intact o volume of urine should not be below the obligate urine volume
loss o ability of the kidneys to concentrate the urine is still intact o the specific gravity should be elevated o osmolarity should be high
PAUNAWA
Ang trans na ito ay hango mula sa MED Trans ng 2B and 2D 2016 at
mula sa librong Harrisons 18th ed. May ilang mga notes na kasama
ito base sa mga napagusapan sa klase.
creatine phosphokinase
SLEEP DISTURBANCES- first symptom
hindi ginagamit na marker for GFR kasi hindi constant at narereabsorb
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TRANSCRIBED BY: LUKE, LEIA, HAN, CHEWBACCA
Page 2 of 6
Renal Symptoms
Nov. 4, 2013
o urine sodium level should be low o urine acidity there is some form of acidosis
if that is not the case: there is a problem in tubular function: Acute Tubular Necrosis/ Acute Renal Failure
PRE-RENAL AZOTEMIA POST-RENAL AZOTEMIA
single nephron GFR (SNGFR)
GFR of all single nephron is reduced
Normal tubular function
Normal BUN: serum creatinine concentration is 10:1
Elevated ratio also can be produced by the following factors: o Tetracycline administration o Glucocorticoid therapy o Presence of blood in the
gastrointestinal tract o Increased protein turnover
due to trauma or burn
Applied when acute obstruction lowers single nephron GFR (SNGFR) causes azotemia
Causes backflow
Increased pressure
Compression
Renal injury
Acute incomplete obstruction of the ureter and acute glomerular injury also may reduce SNGFR and leave tubule function relatively intact
TUBULAR FUNCTION IMPAIRED
ACUTE RENAL FAILURE
Certain acute renal diseases that produce azotemia
Lower single nephron GFR (SNGFR) and damage the tubules sufficiently
Reduce or even abolish tubules reabsorptive function
Produce acute renal failure
CHARACTERISTICS OF IMPAIRED TUBULAR FUNCTION
Urinary sodium concentration
>20 mmol Usually is 40 mmol/L
Urine-to-plasma (U/P) ratio for urea
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TRANSCRIBED BY: LUKE, LEIA, HAN, CHEWBACCA
Page 3 of 6
Renal Symptoms
Nov. 4, 2013
In glomerular hematuria: RBC exposed to urine Hypo-osmotic urine Decreased osmolarity of the urine Causes the RBCs to shrink: Dysmorphic RBC Count the no. of RBC and the dysmormphic RBC
More than 85%:
Possible Glomerular Hematuria Less than 50%:
Possible tubular hematuria or hematuria outside kidneys (infection, stones, injury etc.)
From 2B 2016 trans:
female ask menstrual cycle
single urinalysis with hematuria is common and can result from: o menstruation o viral illness o allergy o exercise o mild trauma
Gross hematuria o with blood clots o usually not an intrinsic renal process o suggest a postrenal source
Persistent urinalysis o >3 RBCs/HPF on 3 urinalyses, or gross hematuria o associated with significant renal or urologic lesions in 9.1% of
cases
Isolated microscopic hematuria o can be manifested by glomerular diseases
Glomerulonephritis
Na and H2O retention HTN periorbital edema (puffiness oround the eyes) during the
morning
proteinuria
hematuria with dysmorphic RBCs, RBC casts, proteinuria >500 mg/dL (virtually diagnostic)
Total hematuria
occurs evenly throughout voiding
blood has had the opportunity to mix fully with the bladder urine
Isolated Hematuria
bleeding occurs mainly at the beginning or end of micturition
without significant proteinuria, cells, or urinary casts
prostatic or urethral origin is more likely
no significant findings
common causes of isolated hematuria o urinary tract stones o benign and malignant neoplasms of
the urinary tract o tuberculosis o trauma o prostatitis o few primary renal diseases
ABNORMALITIES OF URINE VOLUME
POLYURIA
a urine volume above 3 L/d quantification of urine volume by 24h urine collection results from 2 possible mechanisms:
o excretion of non-absorbable solutes (glucose) o excretion of water (defect in ADH prod. or renal
responsiveness) o distinguished by urine osmolality
300 mosmol/L solute diuresis
Diabetes Insipidus Central: lack ADH
idiopathic 2
o to hypothalamic conditions (posthypophysectomy, trauma,
neoplasm, inflammatory, vascular, or infectious) Nephrogenic: not receptive to the effect of hormones (receptors)
Solute Diuresis eg. Mannitol
Natriuretic Syndromes
Syndromes associated with tubule dysfunction Seen in renal tubular acidosis o May have problems with PROXIMAL TUBULES:
Distal tubule will try to compensate and is unable to compensate and reabsorb all.
(+) diuresis o May have problems with DISTAL TUBULES:
Normal functioning proximal tubule but the distal continues to excrete excess urine volume.
o May cause: Loss of Sodium Inability to reabsorb nutrients, sugar, vitamins Cannot maintain acid base balance: Metabolic Acidosis
PRIMARY POLYDIPSIA
cause: unknown increase fluid intake results from habit, psychiatric disorder, neurologic lesions or
medications
NOCTURIA
Occurs during: Reduced renal osmotic concentration High sodium excretion Solute diuresis Low bladder capacity.
More than twice Possibility: may also have polyuria
OTHER RENAL MANIFESTATIONS
Dysuria Pain or a burning sensation during urination
Urinary frequency
Voiding at frequent intervals
Due to a sense of bladder fullness because of an irritable bladder that feels full even when it is not
Urgency Exaggerated sense of needing to urinate
Due to an irritable or inflamed bladder
Enuresis
Involuntary passage of urine at night or during sleep hence the synonym bed-wetting
Bed-wetting without gross urologic abnormalities
Incontinence
Inability to retain urine in the bladder
Results from neurologic or mechanical disorders of the system that controls normal micturition
Overflow Incontinence
The inability to control urination. Unable to completely empty the bladder
leading to overflow, which leaks out unexpectedly
Hirsutism
Male-pattern hair growth Affects approximately 10% of women of
reproductive age FEMALES ONLY
Virilization
State in which androgen levels are sufficiently high
Cause the following signs and symptoms: o Deepening of the voice o Breast atrophy o Increased muscle bulk o Clitoromegaly o Increased libido
Ominous sign that suggests the possibility of an ovarian or adrenal neoplasm
CLINICAL MANIFESTATIONS OF GLOMERULAR DISEASE
Asymptomatic Proteinuria 150mg-3g/d Hematuria > 2RBCs/HPF in spun
urine
Macroscopic Hematuria Brown or red painless hematuria Usually coincides with intercurrent
infection Asymptomatic Hematuria or proteinuria in between
attacks
Nephritic Syndrome Oliguria Proteinuria usually 3g/d Small kidneys
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TRANSCRIBED BY: LUKE, LEIA, HAN, CHEWBACCA
Page 4 of 6
Renal Symptoms
Nov. 4, 2013
Rapidly Progressive Glomerulonephritis
(RPGN)
Renal failure over days or weeks Proteinuria usually 3.5g/d Increased cholesterol Decreased albumin Lipiduria
DIFFERENCE BETWEEN NEPHROTIC AND NEPHRITIC
Features Nephrotic Nephritic
Onset Insidious Abrupt
Edema ++++ ++
BP Normal Raised
JVP Normal or low Raised
Proteinuria ++++ ++
Hematuria May or may not occur +++
RBC Casts Absent Present
Albumin Low Normal / slightly decreased
edema in nephrotic syndrome is d/t massive proteinuria
TUBULOINTERSTITIAL DISEASES
Characterized by inflammatory scarring changes
Primarily involves tubules and interstitium
Relative sparing of the glomerulus and vasculature
CLINICAL PRESENTATION
As compared to glomerular causes of kidney diseases, patients with
tubular kidney disease progress in a slow progressive manner:
Slower rate of loss of renal function Less severe systemic hypertension No edema despite severe degree of renal insufficiency Impaired concentrating capacity
(nocturia, polyuria) Glycosuria w/o hyperglycemia Low grade proteinuria Electrolyte imbalance
COMMON CAUSES
1. Drug induced interstitial nephritis (NSAIDs, rifampicin, lithium)
2. Infectious ( viral, bacterial , parasitic) 3. Malignancy (multiple myeloma, lymphoma) 4. Transplant rejection 5. Reflux Nephropathy 6. Obstructive Nephropathy 7. Metabolic (gout) 8. Radiation
CLINICAL ASSESSMENT OF RENAL FUNCTION
Urinalysis
Serum creatinine
Creatinine Clearance
Ultrasound
Radiologic Exam
Electrolytes
CBC
URINALYSIS
In contrast to GFR, urinalysis tells little about the severity of renal disease but may point to a specific diagnosis.
A key feature of the assessment of any patient with renal disease 1. Physical Properties 2. Chemical Properties 3. Microscopy
PHYSICAL CHARACTERISTICS
Normal Values Clinical Values
Color Yellow May point to drug ingestion (rifampicin)
Specific Gravity
1.003 - 1.030 1.000-1.005 in diabetes insipidus
>1.030 due to contrast dyes, glucose, mannitol
Turbidity No clinical significance
Chyluria (milky white) due to fistula between bladder
Due to phosphate precipitation
and lymphatics
CHEMICAL CHARACTERISTICS
Normal Values Comments
Urine pH 4.5-8 (5-6) pH Possible Conditions
5 Uric acid stones 7 Vegetarian diet
8 Systemic acidosis (renal-tubular
acidosis) 7-8 Struvite stones
Urine Protein
Negative ( 500mg/dl
MICROALBUMINURIA
Urine albumin concentration >30ug/min or 30mg/day
Most of the urinary proteins are low molecular weight proteins like Tamm-Horsfall proteins.
ALBUMIN CREATININE RATIO
More accurate method.
Example: ratio of
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TRANSCRIBED BY: LUKE, LEIA, HAN, CHEWBACCA
Page 5 of 6
Renal Symptoms
Nov. 4, 2013
RBC Cast Seen in glomerulonephritis and
sometimes in strenuous exercises
Dysmorphic RBC
Due to longer contact with urine
Dysmorphic RBCs (%)
Possible Origin of Disease
>85 Glomerular
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TRANSCRIBED BY: LUKE, LEIA, HAN, CHEWBACCA
Page 6 of 6
Renal Symptoms
Nov. 4, 2013
INTRAVENOUS UROGRAPHY
Fairly accurate diagnostic procedure when properly done
At 30 min Maximum visualization of the renal parenchyma
At 5 10 min Collecting system, ureters, bladder
Normal IVP showing filling of ureters w/ contrast dye from the pelvis to the bladder.
Showed a delayed nephrogram due to a stone in the left mid ureter
RETROGRADE PYELOGRAPHY
Placement of catheter through urethra by cystoscopy advancing to renal pelvis
Information on possible filling defects, obstructing lesion especially length of obstruction and ureter distal to the obstruction
ANTEROGRADE PYELOGRAPHY
Contrast procedure via percutaneous renal puncture.
TAKE-HOME MESSAGES (2D 2016)
1. Pyuria or presence of pus cells in the urine does not always equate to urinary tract infection. 2. After establishing working diagnosis, we should be able to estimate the degree of renal dysfunction. 3. If the creatinine is 2mg/dl, it is best to refer the patient to a kidney specialist. 4. If with significant proteinuria despite normal creatinine levels, best to refer to a kidney specialist.
2C 2015 NOTES:
25% of cardiac output goes to the kidneys Change in sleeping pattern earliest manifestation of uremia Anorexia, nausea and vomiting more noticeable manifestations of
uremia
Uremia absolute indication for dialysis GFR is dependent on blood flow
Prerenal azotemia tubules are still intact i.e., can still concentrate sodium; maintain electrolyte and acid base balance; but GFR is decreased
Postrenal azotemia due to acute obstruction lowers single nephron GFR (SNGFR)
GI loss most common cause of hypovolemia Prostate cancer most common cause of painless hematuria Acidosis + Urine pH is basic tubule dysfunction Obligate water loss 500 cc/day Increase urine sodium of >20-40mmol/liter despite hypovolemia
acute tubular necrosis (ATN) or acute renal failure (ARF)
Prerenal azotemia fluids may still be excreted Renal failure fluids may not be excreted anymore Cause of bilateral kidney obstruction benign prostatic hyperplasia
(BPH), pregnancy
Oliguria = 3.5g/24hrs or 1.7m2/body surface area massive
proteinuria may lead to nephrotic syndrome Tamm-Horsfall proteins filtered proteins Bence-Jones proteins multiple myeloma Glomerular proteins high molecular weight proteins Hematuria consider prostate or urethral origin Isolated hematuria no proteins, casts, cells in the urine; only
hematuria is present
Central diabetes insipdius decreased ADH Nephrogenic diabetes insipidus increased ADH but the kidneys
are not responsive
Mannitol causes solute diuresis Natriuretic syndromes there is development of renal-tubular
acidosis (RTA)
Primary polydipsia (idiopathic) patient drinks a lot of water polyuria, nocturia
Nocturia in venous insufficiency due to increased preload or increased circulating blood volume
Dysuria there is burning sensation while urinating Crescent formation hallmark of rapidly progressive
glomerulonephritis (RPGN)
Reflux nephropathy there is development of recurrent UTI especially in children; due to congenital diseases
Obstructive nephropathy recurrent UTI not related to STDs Obstruction in the urethra, bladder extrarenal cause Obstruction in the tubules intrarenal cause Intrarenal obstruction usually due to gout leads to uric acid
nephropathy
Chemotherapy destroys a lot of cells will increase uric acid excretion may also obstruct the tubules (intrarenal obstruction)
Pyuria consider glomerulopathies (proliferative)
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