MEDICINE
Approach to Patient with Diseases of the Kidney and Urinary Tract
Lecturer: Dr. Maria Ailsa A. Escobin, MD, FPCP, FPSN
SYNDROMES OF KIDNEY DISEASES
- Kidney diseases usually present as syndromes.
Meaning, it’s a group of signs and symptoms that
gives you a clue to which particular kidney disease it
is being attributed to.
- Therefore, the different signs and symptoms may be
present in different syndromes but the combination
will lead to the specific kidney disease syndrome
- The 10 syndromes are:
1. Acute and Rapidly Progressive Renal Failure
(ARF/RPRF)
2. Acute Nephritis
3. Chronic Kidney Disease
4. Nephrotic Syndrome
5. Asymptomatic Urinary Abnormalities
6. Urinary Tract Infection
7. Renal Tubule Defects
8. Hypertension
9. Nephrolithiasis
10. Urinary Tract Obstruction
ACUTE AND RAPIDLY PROGRESSIVE RENAL FAILURE
- Decline in glomerular filtration rate (GFR) happens
over days (ARF) or weeks (RPRF)
*Acute = Days, Rapid = Weeks, Chronic = 3 to 6 mos.
*Chronic = irreversible, Acute and Rapid = reversible
- Clinical Clues for ARF/RPRF:
› Anuria (absence of urine) or oliguria (decrease
in urine output by <500cc in 24hrs)
 even if your patient is not hydrated and
doesn’t eat, he should put up at least 500cc
of urine a day
› Uremia of recent onset
 Uremia is a constellation of signs and
symptoms involving different organ systems
 May include gastritis, abdominal pain,
anorexia, nausea, vomiting, insomnia,
decrease in sensorium, dizziness or change
in behavior
 If these symptoms happen in days and
weeks, you may have acute uremic
syndrome or acute renal failure
› Edema
 Oliguria or anuria: you are not able to
remove the excess fluid in your body
 Proteinuria: decrease in serum albumin
which decreases oncotic pressure resulting
in edema and sign of congestion
› Hypertension
 Oliguria which increases blood volume then
increasing cardiac output which eventually
increases blood pressure
› Electrolyte imbalances
MEDICINE: Approach to Patient with Diseases of the Kidney and Urinary Tract | 1
Transcriber: Cana Bejasa
Editor: Ica Mastrili
Number of pages: 6
 Because of the decrease in GFR, you are
unable to remove excess Potassium and
Magnesium resulting to hypermagnesemia
and hyperkalemia.
 Those disease entities that peg tubulo-
interstitial places would decrease
electrolytes because of the failure of the
tubules (which are found in the
interstitium) to reabsorb the electrolytes
 Damage to interstitium (where the tubules
are found) will also destroy the function of
these tubules in the reabsorption and
excretion of electrolytes
› Urinary sediments
 For an acute kidney injury, what you see are
casts
- Causes of ARF
› Acute tubular necrosis (ATN)
 Happens when there is decrease in
intravascular volume thus decreasing the
renal perfusion causing ischemia of your
renal cells
 If hypoperfusion is not treated adequately,
it will lead to ATN
 If hypoperfusion is treated immediately, the
decline in GFR is reversed without any
residual renal function and will not lead to
ATN
 (+) Damaged renal parenchyma because of
prolonged hypoperfusion
› Urinary Obstruction
 In elderly men, the most common is bladder
outlet obstruction secondary to benign
prostatic hypertrophy or prostatic CA
› Nephrotoxins
 Aminoglycosides, Antibiotics, Analgesics,
NSAIDs
ACUTE KIDNEY INJURY: there is decline in urine
output but patient is not uremic, not needing renal
replacement therapy
ACUTE KIDNEY FAILURE: uremic and needs renal
replacement therapy
- Causes of RPRF: usually related to glomerular defect
› Most common cause is immune-mediated
› Vasculitis
› Crescentic GN (upon renal biopsy)
 Crescents are formed in the Bowmann’s
space where there is a break in the visceral
epithelium of the capillary loop
 Inflammatory cells in Bowmann’s space
 Irreversible once it undergoes fibrosis
› Hemolytic Uremic Syndrome
› Malignant nephrosclerosis/hypertension
 › Cryoglobulinemia - Clinical Presentation
- Diagnosis › Acute reduction in GFR similar to Acute
› History Renal Failure, also associated with Rapidly
 History of impetigo? Pharyngitis? Progressive Glomerulonephritis
Dehydration? Diarrhea? › Nephritic Urinary Sediments:
› Physical Exam  Dysmorphic Hematuria
 Assess volume status of patient  RBC casts (RBCs that go into the tubules
 Edematous? Dehydrated? because there is a break in the capillary
 Crackles? wall and aggregate)
› Urinalysis  Proteinuria (albumin)
 Most common and cheapest ACUTE: Narrow caliber of casts
 Look for proteinuria, RBCs and WBCs CHRONIC: Wider/Broader
 Pyuria in urinalysis does not always mean › Volume expansion
UTI  Hypertension (volume and sodium
 Problems involving tubulo-interstitial spaces retention)
may give “sterile pyuria”, intake of  Pulmonary congestion (crackles, cardiac
nephrotoxic drugs may give pyuria and not wheeze)
necessarily infection  Facial or peripheral edema
 pH and specific gravity - Causes
› GFR: expensive so may not be done that often › Post-Streptococcal GN
› BUN  Prototype of AGN
› Serum Creatinine  Infection with group A Strep. which
 If short for GFR, request for creatinine and brings about immune complex
compute for Cockcroft-Gault Equation deposition in the glomerular capillary
membrane
 Induces intense yet transient
inflammatory process = resolve in a
**multiply everything by 0.85 if Px is female
matter of 4 to 6 weeks
 Estimating creatinine clearance is used to
 GFR falls but returns to normal within
stage Chronic Kidney Disease (Stage 1 to 5)
weeks or months
 In acute kidney failure, you estimate the
If proteinuria/pyuria persists after 6
GFR to adjust the dose of medications
weeks, it may not be due anymore to Post-
 AGAIN: Acute = Adjust Dosage of Meds
Strep GN. Request for a Renal Biopsy.
Chronic = Staging
› Bacterial or viral infections (Hepa B, Hepa C,
ACUTE NEPHRITIS HIV, Syphilis, Leprosy, Malaria
CAUSES Schistosomiasis)
A. Acute Glomerulonephritis › Lupus nephritis
- Primarily affects the glomeruli but to a lesser › Membranoproliferative Glomerulonephritis
extent the renal tubules may also be involved › Henoch-Schonlein Purpura
- Immune-mediated inflammation of the  Similar to Berger’s but has more
glomerulus systemic symptoms like abdominal pain
- Primary vs. secondary  In younger age group
› Primary/Idiopathic › IgA nephritis or Berger’s Disease
 Inflammation is localized in the kidney  Most common manifestation is Painless
 EXAMPLES: Minimal Change Disease, Hematuria
Membranoproliferative  Happens during or after an URT
Glomerulonephritis, IgA Nephropathy infection (pharyngitis)
› Secondary - Renal Biopsy
 Caused by other diseases extending to › Usually required for a definitive diagnosis
the kidney and to determine whether ARF/RPRF exists
 EXAMPLES: Lupus Nephritis, Diabetic › Proliferative GN (RPGN with crescents)
Nephropathy from DM, NSAIDs, Post- often with extracapillary crescent formation
Strep GN, HPN › Treatment and prognosis depend on the
- Damage to the glomerular wall allowing RBC definite histologic pattern and types on
and plasma cells to enter the urinary space to immune complex and immunoglobulins that
the proximal tubule and into the urine. Thus, are deposited in the renal tissue
the RBCs in the urine are dysmorphic.

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 › LIGHT MICROSCOPY: Pattern and
architecture of interstitium and glomerulus
› IMMUNOFLUORESCENCE: sample is given
antibodies to Ig’s and the ones that light up
are those that deposit in the renal
parenchyma
 (+) C3 and IgG = Lupus
 (+) IgA = IgA Nephropathy
 (+) IgG, IgM and C3 = Anti-glomerular
basement membrane antibody disease
› ELECTRON MICROSCOPY: observe
basement membrane and see what
deposits are there
 Subepithelial Deposit: Membranous GN
 Subepithelial “Humps”: Post-Strep GN
B. Acute Tubulointerstitial nephritis
- Inflammation limited to the renal interstitium
- Inflammatory changes limited to the renal
interstitium but may also affect glomerulus
- Evidence of tubule cell injury : electrolyte and
water imbalances
- Hematuria, RBC casts, reduction in GFR, lesser
proteinuria compaired to AGN
- Leukocyturia (eosinophiluria) with peripheral
blood eosinophilia are common
- Causes
1. Infections
a. Bacterial
› Acute Pyelonephritis
› Rocky Mountain Spotted Fever
b. Viral
› Cytomegalovirus
2. Drugs
› Analgesic Nephropathy
› Lithium Nephropathy
3. Metabolic Causes
› Hypokalemia, Hypercalcemia
nephropathy
› Urate nephropathy
› Oxalate Nephropathy
4. Other Causes
› Heavy metals
› Reflux nephropathy
› Obstructive nephropathy: Reflux of
urine back to the kidneys
› Neoplastic diseases
› NSAIDs
- Clinical Features of Acute Drug-Induced TIN
› Signs and Symptoms (Allergic in nature)
 Fever (85-100%)
 Maculopapular Rash (25-50%)
 Arthralgias
 Uremic Symptoms: if GFR is ↓
› Laboratory Findings
 Hematuria (95%)
 Eosinophilia (80%)
 Sterile pyuria
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 Low-grade proteinuria (not albumin
but hyaline cast or Tamm-Horsfall
Protein)
 Eosinophiluria
 WBC casts
CHRONIC KIDNEY DISEASE
- PROGRESSIVE AND IRREVERSIBLE destruction of
nephrons resulting in reduction in GFR for at least 3
to 6 months regardless of cause
- Proofs of Chronicity
› Bilaterally small kidneys upon ultrasound
 except on diseases that are infiltrative in
nature like Multiple Myeloma,
Sarcoidosis, Amyloidosis, DM
 Loss of corticomedullary differentiation
and thinning of the cortex
› Renal osteodystrophy (Mineral Bone Disease):
brought about by changes in Calcium and
Phosphorus levels
› Symptoms of uremia
 Slow, insidious onset
› Broad casts on urinalysis
 Tubules become atrophic, producing
larger lumer, thuse larger diameter of the
casts
- Nonspecific evidences of chronicity in renal failure
› Anemia of normocytic-normochromic type
 (+) ↓ Iron levels: anorexia, vomiting,
nausea or decreased intake of Iron
› Hyperphosphatemia
› Hypocalcemia
› Proteinuria
- Clinical Features
› Dermal: pruritus, easy bruisability, edema
› CVS: dyspnea on exertion, retrosternal pain on
inspiration (pericarditis)
› GIT: anorexia, nausea, vomiting
› GUT: nocturia, oliguria, impotence
› Neuromuscular: restless legs, irritability,
inability to concentrate, insomnia, decreased
libido
- Physical Exam Findings
› General: sallow, debilitated appearance
› Dermal: pallor, ecchymoses, excoriations,
edema, xerosis
› HEENT: uriniferous breath
› Pulmonary: rales, pleural effusion, dyspnea
› CVS: hypertension, flow murmur or pericardial
friction rub, cardiomegaly
› Neurologic: stupor, asterixis, myoclonus,
neuropathy
- ARF on top of CKD
› The acute component of the renal failure must
be evaluated as this is potentially reversible
› In can also happen that you have a patient with
chronic kidney disease with stable renal
 function but suddenly developing rise in - Mild hematuria, pyuria, and cast or subnephrotic
creatinine or decline in GFR proteinuria with no evidence of other nephrologic
› Common causes of acute deterioration of renal syndromes
function: - “Subnephrotic”: Less than 2 grams
 Volume depletion - if there are no fever, dysuria or CVA tenderness then
 Urinary tract obstruction the patient, most likely, has no infections
 Drug-induced nephrotoxicity - Isolated Hematuria
 Exacerbation of underlying renal disease › Clue to:
 Neoplasm (Malignancy in the bladder or
NEPHROTIC SYNDROME
prostate), stone, infection in any part of
- Proteinuria of >3.5g/1.73 m2 surface area in 24
the urinary tract
hours of mainly albumin
 Analgesic and sickle cell nephropathies
- Hypoalbuminemia (< 3.5 g/dl)
› Diagnostics
- Edema and anasarca
 Ultrasound
- Hypercholesterolemia (> 200 mg/dl)
 Intravenous Pyelogram
- Lipiduria
 Cystoscopy
- Massive proteinuria alone has come to define the
 Renal arteriography
syndrome, since this finding connotes a serious
› Nephronal Hematuria
renal disease whether or not the protein losses lead
 RBCs come from glomerulus
to hypoalbuminemia, lipid disturbances, or edema.
 urinary casts contains RBC or Hgb
- Causes
pigment indicating damage to the
› Minimal Change Disease (most common in
nephron
children, also known as Nil Disease)
› Nephronal Hematuria w/ Proteinuria
› Idiopathic Membranous glomerulopathy
 Suggests a worse prognosis with high
› Focal and Segmental Glomerulosclerosis
tendency to progress to chronic renal
› Diabetic nephropathy (most common secondary
failure
nephrotic syndrome)
- Isolated Proteinuria
- Primary Nephrotic Syndrome may be due to:
› Indicates little or no inflammatory reaction
› Orthostatic or postural proteinuria (benign)
within the glomeruli as in Diabetes Mellitus and
› Membranous glomerulonephritis
amyloidosis
› Idiopathic Membranoproliferative
- Pyuria (Leukocyturia)
Glomerulonephritis
› Usually reflect infection and inflammation of
› Focal Segmental Glomerulosclerosis
the lower urinary tract rather than parenchymal
› IgA nephropathy
renal disease
› Minimal Change Disease
› May be present in:
› Proliferative GN
 Tubulointerstitial nephrits
- Secondary Nephrotic Syndrome may be due to:
 Lupus nephritis
› Hereditary-familial: DM (most common),
 Pyelonephritis
Alport’s syndrome, sickle cell disease
 renal transplant rejection
› Autoimmune: SLE, Goodpasture’s syndrome,
› WBC cast establishes the kidney as the site of
Wegener’s granulomatosis, Polyarteritis
inflammation
Nodosa, Rheumatoid Arthritis
› Causes of Sterile Pyuria
› Infectious: Postinfectious GN, endocarditis,
 Recent bacterial urinary infection being
hepatitis B, hepatitis C
treated with antibiotics
› Drug-induced: NSAIDs, heroin, gold, Hg
 Glucocorticoid therapy
› Neoplastic: Hodgkin’s disease, lymphomas,
 Acute febrile episodes
leukemia, Multiple Myeloma
 Cyclophosphamide administration (SLE)
- Clinical Features
 Pregnancy
› Edema and anasarca leading to dyspnea
 Genitourinary trauma
because of the pleural effusion
 Prostatitis and cystourethritis
› Urine contains fewer cellular elements
 All forms of Tubulointerstitial nephrits
› Acute changes in GFR and urine volume are
- Usual Infections of Persistent Sterile Pyuria (look
uncommon
for infections that don’t really involve the kidney)
› Hematuria may or may not be present
› TB
ASYMPTOMATIC URINARY ABNORMALITIES › Fungi
- Patient doesn’t have any other symptoms except an › Atypical mycobacteria
abnormality in the urinalysis › Haemophilus influenzae

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 › Anaerobic or fastidious bacteria Cloudy/foul
Yes Yes/No
smelling urine
URINARY TRACT INFECTION
- Demonstration in urine of pathogenic organism: DIAGNOSTIC PRESENTATION
› bacterial colony counts >105 organisms/ml urine Sepsis: Presence of any two of the following
› >102 colonies/ml in symptomatic patients and › Temperature >380C or < 360C
urine obtained by suprapubic aspiration or › Leucopenia (WBC< 4,000) or Leukocytosis (WBC >
bladder catheterization 12,000)
› Even if your urinalysis is midstream and the › Tachycardia (HR>90 beats/min)
growth is just <105, if your patient is › Tachypnea (RR> 20/min or PaCO2 <32mmHg)
symptomatic then that is already UTI › Hypotension (SBP< 90mmHg or >40mmHg drop from
- Clinical Manifestations as to Site of Involvement baseline)
› Bladder & Urethral Inflammation: dysuria,
frequency, urgency and suprapubic tenderness Acute
Acute cystitis
› Prostatitis: frequency, dysuria, urgency with Pyelonephritis
prostate that is boggy and tender Urinalysis
Yes Yes
› Renal Parenchymal Infection: (infection has Dipstick for
(if with signs of (pyuria >5
leukocyte
already ascended to the kidneys so there are vaginal discharge wbc/hpf of
esterase and
systemic manifestations of the infection) flank or irritation) centrifuged urine)
nitrates
pain, chills, fever, nausea and vomiting, Yes Yes
Urine gram
hypotension from sepsis and leukocyte casts (if no response (>10,000cfu/mL)
stain and
after 3 days of *before giving
WHO ARE AT RISK OF DEVELOPING UTI? culture
antibiotic) antibiotics
1. Gender Yes if suspecting
Blood culture No
› Female – proximity of urethra to the anus sepsis
› 50-60% of adult women report that they have
had UTI DIAGNOSTIC TEST
› Affects 1-3% of female school children - Post-treatment urine culture to confirm eradication
› Sexual intercourse 3x a week is associated with of bacteriuria and resolution of infection
2.6 times greater risk of UTI because of the - If with PN, recurrent UTIs, concurrent GDM,
pressure on the urinary bladder nephrolithiasis or urolithiasis, and pre-eclampsia, do
› Pregnancy urine culture monitoring at monthly intervals until
2. Abnormality in the urinary tract due to: delivery to ensure that urine remains sterile during
› Enlarged prostate pregnancy
› Stones
› Vesicoureteral reflux (school children) Acute
Acute cystitis
› Neurogenic bladder (those with longstanding Pyelonephritis in
in Pregnancy
Pregnancy
Diabetes and spinal injuries)
Urine
3. Immunocompromised state gram satin Yes Yes
› Diabetes and (first line test) (>10,000cfu/mL)
› Lupus culture
› Post-transplant patients Yes (as alternative)
Urinalysis
› With underlying kidney disease >8 wbc/mm3 of Yes
Leukocyte
› Patients taking immunosuppressant uncentrifuged urine (pyuria > 5 wbc/hpf
estrase
OR of centrifuged
4. Indwelling catheter and
> 5 wbc/hpf of urine)
Nitrates
CLINICAL PRESENTATION centrifuged urine
Blood
Same clinical presentation of acute cystitis and No Yes if with sepsis
culture
Acute pyelonephritis in pregnanct and non pregnant. Post
treatment
Acute Yes Yes
Acute cystitis urine
pyelonephritis
culture
Dysuria Yes Yes/No
Urgency/frequency Yes Yes/No
RECURRENT UTI
Perineal Flank
Pain suprapubic (+) CVA - episodes of acute uncomplicated cystitis
lower back tenderness documented by urine culture occurring > 2x /year in
Gross hematuria Yes/No Yes/No a non-pregnant woman with no known urinary tract
Fever /chills No Yes abnormality
Nausea/vomiting No Yes
MEDICINE: Approach to Patient with Diseases of the Kidney and Urinary Tract | 5
DIFFERENTIAL DIAGNOSIS › Visualization by x-ray
- for women, differentiate urethritis and UTI › Removed by surgery or cystoscopy
- Urethritis - Suggestive of Diagnosis:
› history of STD, new sexual partner › Renal colic
- Vaginitis › Painful hematuria
› presence of vaginal discharge, pruritus,  Males: Radiates to scrotum
dyspareunia  Females: Radiates to inguinal area
› absence of frequency and urgency  Pain stops when the stone doesn’t move
› Unexplained pyuria, dysuria and frequency
RENAL TUBULE DEFECTS
- This syndrome encompasses a large number of COMPOSITION OF RENAL STONES
acquired and hereditary disorders, all of which tend › Calcium oxalate
to affect renal tubules more than glomeruli › Uric Acid
- Impairment of secretion and/or reabsorption of › Cystine
electrolytes and organic solutes and limit urinary › Struvite: associated with infection
concentrating and diluting ability All are radiopaque except for uric acid stones and are
- Polyuria, nocturia, metabolic acidosis, and various visible in routine abdominal radiography.
disorders of the fluid and electrolyte balance
URINARY TRACT OBSTRUCTION
HEREDITARY ANATOMIC DEFECTS ANURIA
- Polycystic kidney disease, medullary cystic disease - Obstruction of the bladder outlet
and medullary sponge kidney - Blockage of upper urinary drainage from both
- Hematuria, bacteriuria, flank pain, or unexplained kidneys or from a solitary functioning kidney
azotemia
- Detected by ultrasonography or intravenous BLADDER OUTFLOW OBSTRUCTION
pyelography - Large bladder after voiding
- Palpable in hypogastric area
TUBULE TRANSPORT DYSFUNCTION - Nocturia, frequency, overflow incontinence, slowing
Three Patterns of Renal Dysfunction: or hesitancy of micturition
a. Proximal Tubular Dysfunction - CAUSES: Urethral stricture, tumor, stone,
› Renal Tubular Acidosis type II w/ or w/o neurogenic causes, prostatic hypertrophy
Fanconi’s syndrome (most prominent)
› ↓ in reabsorption of electrolytes  urine UPPER TRACT OBSTRUCTION
› Glucosuria and amino-aciduria (not all - Few symptoms especially when obstruction is
glucosuria are due to diabetes) incomplete and unilateral
b. Distal Tubular Dysfunction - Normal volume of urine or even increased because
› Renal Tubular Acidosis type I, salt wasting, or of defect in the renal concentrating function
hyperkalemia - If you have kidneys and only one ureter is
› DM and Lupus nephritis obstructed, the other kidney compensates by
c. Renal Medullary Dysfunction producing a lot of urine. The urine is usually diluted
› Decreased concentrating ability with polyuria & and has less sediments
nocturia - Normal or even increased urine output
› Very diluted and voluminous urine, nocturia
URINARY TRACT OBSTRUCTION
HYPERTENSION - Urinary Stasis secondary to obstruction predisposes
- Blood pressure > 140/90 on 2 separate office visits to recurrent urinary tract infection
- Chronic urinary obstruction predisposes to
JNC VII Classification
progressive loss of renal function
BP Systolic BP Diastolic BP
Classification (mm Hg) (mm Hg) END
Normal < 120 < 80
Prehypertension 120 – 139 80 – 89 “Makinig ka sa tula ko na tungkol sa gago na kapuna-puna
Stage 1 na mukhang kabado na. Takpan mo yang mukha mong
140 – 159 90 – 99
Hypertension
kasuka-suka. Gwapo ka sana kung aso ka… Kaso tao ka.”
Stage 2
> 160 > 100 - Loonie, FliptopBattles
Hypertension

NEPHROLITHIASIS
- Definitive Diagnosis:
› Passage of stone

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