Nephrology: Chronic Kidney Disease

Lecturer: Edgardo P. Fajardo, MD

Transcriber: Patrick Angelo R. Bautista March 2020

References and Legends
• {💻} Department of Medicine Powerpoint and {⏯} Discussion
• {📖} Chapters 305 Harrison’s Principles of Medicine 20th Ed. • Eventually, these short-term adaptations of hyperfiltration and
Table of Contents
I. Chronic Kidney Disease
o Pathophysiology
o CKD 4 Steps of Patient Assessment
o Uremia
o Clinical Manifestations of CKD
§ Fluid, Electrolyte, and Acid Base Disorders
§ Disorders of Calcium and Phosphate Metabolism
§ Cardiovascular Abnormalities
§ Hematologic Abnormalities
§ Neuromuscular Abnormalities
§ Gastrointestinal and Nutritional Abnormalities
§ Endocrine-Metabolic Disturbances
§ Dermatologic Abnormalities
o Evaluation and Management of Patient with CKD
I. CHRONIC KIDNEY DISEASE {Ch. 305 📖}
Chronic Kidney Disease
• encompasses a spectrum of pathophysiologic processes
associated with abnormal kidney function and a progressive
decline in glomerular filtration rate (GFR)
Chronic Renal Failure
• continuing significant irreversible reduction in nephron number
and typically corresponds to CKD stages 3-5.
End-Stage Renal Disease (Stage 5 CKD)
• represents a stage of CKD where the accumulation of toxins, fluid,
and electrolytes normally excreted by the kidneys leads to death
unless the toxins are removed by renal replacement therapy,
using dialysis or kidney transplantation.
CKD Defined (NFK K/DOQI-US)
• Kidney damage for more than three months, as defined by
structural or functional abnormality of the kidney with or without
decreased GFR, manifest as either:
o Pathological Abnormalities
o Markers of kidney damage (proteinuria, abnormal urine
sediment, abnormal renal imaging)
§ GFR <60ml/min/1.73m2 for 3 months, with or without
kidney damage
• The responses to reduction in nephron number are mediated by
vasoactive hormones, cytokines, and growth factors.
hypertrophy to maintain GFR become maladaptive as the increased
pressure and flow within the nephron predisposes to distortion of
1 glomerular architecture, abnormal podocyte function, and disruption
1 of the filtration barrier leading to sclerosis and dropout of the
2 remaining nephrons.
3 • Increased intrarenal activity of the RAAS appears to contribute both
3 to the initial compensatory hyperfiltration and to the subsequent
3 maladaptive hypertrophy and sclerosis.
4 • This is why a reduction in renal mass from an isolated insult may
4 lead to a progressive decline in renal function over many years
4
5
Discussion Notes: {⏯}
5
• How would you assess “adaptive hyperfiltration”?
5
5 o Urinalysis – check for protein
6 o Albuminuria – #1 clue that you have a CKD. Since there is
hyperfiltration, there will be decreased albumin causing a shift
in the oncotic pressure. Water will go to the interstitial spaces.
§ Symptoms: edema; anasarca if whole body
§ Early morning edema: periorbital
§ Later in the afternoon: lower extremities
• How would you assess “maladaptive response”? What would
you request to identify if there is “sclerosis”?
o KUB Ultrasound: fibrosis, sclerosis → kidney shrinkage
o Small sized / contracted kidney is a sign of chronicity
(differentiates Acute RF from Chronic RF)
o The different causes of kidney disease will have
contracted / small sized kidneys EXCEPT for the following:
1 Diabetes nephropathy
2 Polycystic Kidney Disease
3 Amyloidosis
4 Multiple myeloma
5 HIV nephropathy
o Normal Kidney Size: ≥9 cm (depending on the height)
o Normal Cortical Thickness: ≥1 cm

Pathophysiology {📖}
involves two broad sets of mechanisms of damage:
1 initiating mechanisms specific to the underlying etiology
o ex. abnormalities in kidney development or integrity, immune
complex deposition and inflammation in certain types of
glomerulonephritis, or toxin exposure in certain diseases of
the renal tubules and interstitium
2 hyperfiltration and hypertrophy of the remaining viable
nephrons, that are a common consequence following long-term
reduction of renal mass, irrespective of underlying etiology and
lead to further decline in kidney function CKD Working / Clinical Definition {💻/KDIGO 2012}
• CKD is defined as abnormalities of kidney structure or function,
present for >3 months, with implications for health
• CKD is classified based on
o Cause
o GFR category
o Albuminuria category (CGA)

• {⏯} we determine the extent of albuminuria because the earliest

sign of kidney damage is albumin spillage. Creatinine will only
increase if 40% of the kidney is already damaged.

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Criteria for CKD (Either of the following present for >3 months) STEP 3: Determine the GFR
Markers of • Albuminuria Evaluation of GFR
Kidney Damage • Urinary sediment abnormalities • Use serum creatinine and a GFR estimating equation for initial
(1 or more) • Electrolyte and other abnormalities due to assessment
tubular disorder • Clinicians should:
• Abnormalities detected by histopathology o Use GFR estimating equation to derive GFR from serum
• Structural abnormalities detected by imaging creatinine rather than relying on serum creatinine alone
• History of kidney transplantation o Understand the clinical settings where eGFR is less accurate
Decreased GFR GFR <60 mL/min/1.73m2 • Do actual clearance measurement (radionuclide GFR scan)

{⏯} In CKD patients, all electrolytes are increased because they
cannot be excreted hence, are retained in the circulation. EXCEPT:
• Sodium – due to volume overload → dilutional hyponatremia
• Calcium – due to 2° hyperparathyroidism
GFR Categories in CKD
Relationship between SCr and GFR
• Serum creatinine is a poor predictor of GFR
• {📖} The normal annual mean decline in GFR with age from the peak
GFR (~120 mL/min per 1.73 m2) attained during the third decade of
life is ~1 mL/min per year per 1.73 m2
o reaching a mean value of 70 mL/min per 1.73 m2 at age 70

4 Steps in Patient Assessment {💻}

STEP 1: Evaluate if your Patient has CKD

Estimating GFR: MDRD and Cockcroft Gault
Evaluate Chronicity
• If GFR is <60 mL/min/1.73 m2 or with markers of kidney damage,
review PMH and previous measurements to determine duration
o If >3 months, CKD is confirmed
o If not >3 months or unclear, CKD is not confirmed (may have
CKD, AKI or both; repeat test accordingly)

STEP 2: Determine the Cause of CKD

• Evaluate the clinical context, including personal and family history,
social and environmental factors, medications, PE, lab measures,
imaging and pathologic diagnosis to determine the causes of
kidney disease
2009 CKD-EPI Creatinine Equation
Risk Factors for CKD
• Hypertension, Diabetes
• Autoimmune disease
• Old age
• African ancestry
• Family history of renal disease
• Previous episode of ARF
• (+) proteinuria, abnormal urinary sediment or structural
abnormality of the urinary tract

Etiology of ESRD (Philippine Data)

Etiology Frequency
Diabetes 44.6%
Hypertension 23.6%
Glomerulonephritis 19.3%
Others 12.5%

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STEP 4: Measure Albuminuria Uremia
Test to detect and measure Albuminuria Uremic toxins
a. Dipstick Testing • Products of nitrogenous metabolism, guanidino compounds
o most commonly used • Products of bacterial metabolism as aromatic amines, and
o Highly specific (97-100%) skatoles
o Not sensitive (32-46%) • Urea and breakdown products
o False negatives: • Compounds retained in circulation, or underproduced
§ Diluted urine o Earliest – gastrointestinal manifestation (nausea and
§ Mild protein loss vomiting), loss of appetite – start dialysis
o Useful only when urine protein exceeds 300-500 mg/day (or o Multisystemic involvement – neurological, cardio – start
albumin >10-20 mg/day) dialysis
o It is essential to know how much protein is excreted to
predict long-term prognosis. Biochemistry of Uremia
• Urea and Creatinine
b. 24-hour measurement o Most commonly used marker of renal excretory function
o gold standard; difficult to collect o Incomplete surrogate markers
o simultaneous urine creatinine o Do not account for the many s/s of uremia
§ to assess completeness of collection • Uremia… Spheres of dysfunction
o Men: 19-26 mg/kg/day o Consequent to accumulation of toxins
o Women: 14-21 mg/kg/day o Consequent to loss of other renal functions
§ Fluid and electrolytes
c. Spot Urine Sampling § Hormones
o Protein-Creatinine Ratio: good correlation with 24-hour o Progressive systemic inflammation and its vascular and
values (r2=0.97) nutritional consequences
§ ≤ 0.2 normal § MIA/ calcification syndrome
§ ≥ 3.5 nephrotic range
o Albumin-Creatinine Ratio: Correlates well with 24-hour Clinical Manifestations of CKD
albumin excretion
§ <30 mg/gm = normal a. Fluid, Electrolyte, and Acid-Base Disorders {💻+📖}
§ 30-300 mg/gm = microalbuminuria Sodium and Water Homeostasis
§ >300 mg/gm = overt nephropathy • Total body Na+ and H2O increased
• Due to disruption of glomerulotubular balance
Evaluation of albuminuria • ECFV expansion → HTN → accelerated nephron injury
• We suggest using the following measurements for initial testing of o Salt/water restriction
proteinuria (in descending order of preference, in all cases an o Loop diuretic +/- Metolazone: may be helpful in loop diuretics
early morning urine sample is preferred): resistance as well as use of higher doses loop
1. urine albumin-to-creatinine ratio (ACR) o Dialysis: indicated in patients with intractable edema and
2. urine protein-to-creatinine ratio (PCR) hypertension in advanced CKD
3. reagent strip urinalysis for total protein with automated reading • Impaired renal conservation of Na+ & H2O
4. reagent strip urinalysis for total protein with manual reading o Filtered Na+ inadequately reclaimed → ECFV depletion →
Acute-on-Chronic renal failure
§ When an extrarenal cause for fluid loss is present, these
patients may be prone to ECFV depletion because of the
inability of the failing kidney to reclaim filtered sodium
adequately. Furthermore, depletion of ECFV can further
compromise kidney function through underperfusion, or a
“prerenal” state, leading to acute-on-chronic kidney failure.
o Cautious fluid repletion with normal saline
§ as well as holding or adjusting the diuretic dose may return
the ECFV to normal and restore renal function to baseline.

Potassium Homeostasis
• Defense against hyperkalemia
o Increase urinary K+ secretion – aldosterone dependent
o Augmented K+ secretion in GI tract
• Precipitants of hyperkalemia
o Increase intake, protein catabolism, hemolysis, hemorrhage
o Metabolic acidosis, Blood transfusion of stored RBC
o Drugs (ACEi, ARB, spironolactone)
• Hypokalemia in CKD
o Very low K+ intake
CKD Progression o Diuretic therapy
• Assess GFR and albuminuria at least annually in people with CKD. o GI losses
Assess GFR and albuminuria more often for individuals at higher o Renal K+ wasting
risk progression, and/or where measurement will impact o Fanconi’s syndrome
therapeutic decisions. o Renal tubular acidosis (RTA)
o Tubulointerstitial disease

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Metabolic Acidosis c. Cardiovascular Abnormalities {💻+📖}
• ↓ ammonia production → ↓ protein excretion → Non-Anion-gap • Leading cause of mortality & morbidity
Acidosis • Risk of CVD in CKD is 10- to 200-fold
• With worsening renal function, the total urinary net daily acid • 30-50% of CKD Stage 5 has advanced CV complications
excretion is usually limited to 30–40 mmol, and the anions of
retained organic acids can lead to Anion-gap metabolic acidosis. Ischemic Vascular Disease
• Net effect: Net protein catabolism → malnutrition • Coronary, cerebrovascular and peripheral vascular
• Start alkali supplementation when HCO3 falls <20-23 mmol/L • Traditional “classic” risk factors:
o Consider need for diuretic o HTN, hypervolemia, dyslipidemia, sympathetic overactivity,
hyperhomocysteinemia
b. Disorders of Calcium and Phosphate Metabolism {💻+📖} • Non-traditional “CKD-related” risk factors:
Bone Manifestations of CKD can be classified into one of the o Anemia, hyperphosphatemia, hyperparathyroidism, sleep
following or most often combinations: apnea, generalized inflammation
• Reduced Renal Function → “Inflammatory State” → Accelerated
a. High bone turnover
vascular occlusive disease and rapid vascular calcification (with
o with increased PTH levels
low fetuin level) → “Attenuated Coronary Reserve”
o Osteitis fibrosa cystica – classic lesion of 2° HPT
o Inflammatory State: High CRP, Low Albumin, Low fetuin
o Clinical Manifestations:
o Attenuated Coronary Reserve: Low NO, Reactive O2
§ Bone pain and fragility § Muscle weakness
species, Dialysis hypotension and hypovolemia
§ Brown tumors § Fibrosis of cardiac muscles
§ Compression syndromes § Constitutional symptoms
Heart Failure
§ Erythropoietin resistance*
• Causes of HF or even pulmonary edema:
b. Osteomalacia o myocardial ischemia
o due to reduced action of the active forms of Vitamin D o left ventricular hypertrophy
o accumulation of unmineralized bone matrix o cardiomyopathy
o Vit D deficiency, Aluminum toxicity, Metabolic acidosis o salt and water retention
c. Low bone turnover • Can be diastolic, systolic dysfunction, or both
o with low or normal PTH levels • “low pressure” pulmonary edema
o Adynamic bone disease o shortness of breath
§ characterized by reduced bone volume & mineralization o CXR: “bat wing” distribution of alveolar edema fluid
§ may result from excessive suppression of PTH production, o absence of ECFV overload
inflammation, or both o normal pulmonary capillary wedge pressure (PCWP)
§ Complications: ↑ incidence of fracture & bone pain and o ↑ permeability of alveolar capillary membranes due to uremia
an association with ↑ vascular & cardiac calcification* o responds to dialysis

Treatment Hypertension and Left Ventricular Hypertrophy

• Phosphate binders • one of the most common complications of CKD
o Ca carbonate, Ca acetate – Ca-based PO4 binders • usually develops early during the course of CKD and is
§ increase total body calcium associated with adverse outcomes including LVH and a more
§ Side effect: hyper-Ca especially in low-turnover bone disease rapid loss of renal function
o Sevelamer and Lanthanum – non-Ca-based PO4 binders • Causes of absence of hypertension in CKD:
§ do not predispose CKD patients to hypercalcemia and may o Salt-wasting nephropathy
attenuate Ca deposition in the vascular bed o Effect of antihypertensives
• Calcitriol and Vit D analogues (Paricalcitol) o Volume depletion
o direct suppressive effect on PTH secretion o Poor LV function
o also indirectly suppresses PTH secretion by raising ionized Ca • “reverse causation” – low BP has worse prognosis than high BP
o may result in hypercalcemia and/or hyperphosphatemia • Management of Hypertension in CKD
o Analogues (Paricalcitol) suppress PTH secretion with less o Overall goals:
attendant hypercalcemia § Slow progression of renal disease
• Calcimimetic agents (Cinacalcet) § Prevent extrarenal complications of HTN (CVD, stroke)
o enhance sensitivity of PT cell to the suppressive effect of Ca o Targets:
• Recommendation: Target PTH between 150-300 pg/mL § 130/80 mmHg
o recognizing that very low PTH levels are associated with § CKD with DM or proteinuria >1 gm/d – 125/75 mmHg
adynamic bone disease and possible consequences of fracture
o Agents:
and ectopic calcification
§ Salt restriction & diuretics – first choice
§ ACEi, ARB - Slow rate of decline
§ Kaliuretic agents – to prevent hyperkalemia

d. Hematologic Abnormalities {💻+📖}

Anemia
• A normocytic, normochromic anemia is observed as early as
stage 3 CKD and is almost universal by stage 4.
• Adverse Pathophysiologic Consequences:
o Decreased tissue O2 delivery & utilization
o Increased Cardiac Output
o Ventricular dilatation and hypertrophy
• Clinical Manifestations:
o Fatigue, diminished exercise tolerance
o Angina, Heart failure
o Decreased cognition and mental acuity
o Impaired defense against infection

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• Peripheral Neuropathy
o usually becomes clinically evident at stage 4 CKD
o sensory nerves involved more than motor
o lower extremities more than upper
o distal parts of extremities more than proximal
• Restless Leg Syndrome
o characterized by ill-defined sensations of sometimes
debilitating discomfort in the legs and feet relieved by frequent
leg movement
• Evidence of peripheral neuropathy without another cause
(diabetes mellitus) is an indication for starting RRT.
• Many of the complications described above will resolve with
dialysis, although subtle nonspecific abnormalities may persist.

f. Gastrointestinal and Nutritional Abnormalities {💻+📖}

Anemia (continuation) • Uremic Fetor
• Treatment o a urine-like odor on the breath, derives from the breakdown of
o Recombinant EPO (Darbopoietin) urea to ammonia in saliva and is often associated with an
§ lessened the need for regular transfusions in severely anemic unpleasant metallic taste (dysgeusia).
CKD patients, thus dramatically reducing the incidence of • Gastritis, peptic disease, and mucosal ulcerations at any level
transfusion associated infections and iron overload as well of the GI tract occur in uremic patients and can lead to:
as prevents the development of alloantibodies that can o abdominal pain, nausea, vomiting, and GI bleeding.
sensitize the patient to donor kidney antigens which makes
• Constipation
renal transplant more problematic.
o worsened by the administration of Ca and Fe supplements
o Iron supplements
• Anorexia, Nausea, Vomiting – due to retention of uremic toxins;
o Folate and Vitamin B12
o protein restriction may be useful
o Recommended Target Hgb concentration: 110-120 g/L
• Weight loss and Protein energy malnutrition
o consequence of low protein and caloric intake
Abnormal Hemostasis
o resistance to anabolic action of insulin & other growth factors
• Patients with later stages of CKD may have:
o often an indication for initiation of RRT
o prolonged bleeding time*
o decreased activity of platelet factor III
g. Endocrine-Metabolic Abnormalities {💻+📖}
o abnormal platelet aggregation and adhesiveness
o impaired prothrombin consumption • Impaired glucose metabolism
• Clinical Manifestations o Slow rate of blood glucose decline after a glucose load
o increased bleeding and bruising o FBS usually normal or only slightly elevated
o prolonged bleeding from surgical incisions o Mild glucose intolerance does not require treatment
o menorrhagia • Elevated plasma insulin level
o gastrointestinal bleeding o Diminished renal degradation of insulin
• CKD patients have a greater susceptibility to thromboembolism o Reduction in insulin dose with worsening renal function
• Treatment o Hypoglycemia
o Reversal of abnormal bleeding and coagulopathy o Many anti-hyperglycemic agents, including the gliptins, require
§ Desmopressin(DDAVP) dose reduction in renal failure; metformin and sulfonylureas are
§ Cryoprecipitate contraindicated when the GFR is less than half of normal.
§ IV conjugated estrogen • Women with CKD
§ Blood transfusion o Low estrogen level
§ EPO therapy o Menstrual abnormalities
§ Optimal dialysis o Infertility and Inability to carry pregnancy to term
o Anticoagulation – prevention of thromboembolism o when GFR 40 mL/min – high rate of spontaneous abortion;
§ Warfarin for atrial fibrillation – decision is made on an with only 20% leading to live births
individual basis in CKD patients because there appears to be o Pregnancy may hasten progression of CKD
a greater risk of bleeding complications • Men with CKD
§ LMWH – avoided or dose adjusted; monitor Factor Xa o Low testosterone
§ Better to use Fractionated Heparin o Sexual dysfunction
§ Aspirin + Dipyridamole o Oligospermia
§ Clopidogrel o Delayed sexual maturation in adolescents

e. Neuromuscular Abnormalities {💻+📖} h. Dermatologic Abnormalities {📖} not discussed

• Well recognized complications of CKD
o CNS, peripheral, and autonomic neuropathy
o abnormalities in muscle structure and function
• Subtle clinical manifestations of uremic neuromuscular disease
usually become evident at stage 3 CKD.
Clinical Manifestations
• Early stage: mild disturbances in memory and concentration,
sleep disturbances
• Later stages: Neuromuscular irritability (hiccups, cramps, twitch)
• Advanced untreated Kidney Failure: Asterixis, myoclonus,
seizures, coma
• Pruritus – common and one of the most vexing manifestations of the
uremic state
• Advanced CKD: even on dialysis, patients may become more
pigmented, and this is felt to reflect the deposition of retained
pigmented metabolites, or urochromes
• Management: rule out unrelated skin disorders and treat
hyperphosphatemia which can cause itch; Local moisturizers, mild
topical glucocorticoids, oral antihistamines, UV radiation
• Nephrogenic Fibrosing Dermopathy
o skin condition unique to CKD patients
o consists of progressive subcutaneous induration, especially on
the arms and legs.
o seen very rarely in patients with CKD who have been exposed to
the magnetic resonance contrast agent gadolinium.

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Clinical Action Plan
Stage Description GFR Action
1 Kidney damage with >90 • Diagnosis and Tx verify the presence of two kidneys, determine if they are symmetric,
normal or ↑ GFR • Tx of comorbidities provide an estimate of kidney size, and rule out renal masses and
• slowing progression evidence of obstruction.
• CVD risk reduction • Because it takes time for kidneys to shrink as a result of chronic
2 Kidney damage with 60-89 Estimating progression
mild ↓ in GFR
3 Moderate ↓ in GFR 30-59 Evaluating and treating
complications
4 Severe ↓ in GFR 15-29 Preparation for RRT
5 Kidney Failure <15 (or Renal replacement Tx
dialysis) (if uremia present)
Evaluation & Management of Px with CKD {not discussed}
History and Physical Examination {💻+📖}
History
• Symptoms and overt signs of kidney disease are often subtle or
absent until renal failure supervenes.
• Particular aspects of Hx that are germane to renal disease include:
o history of hypertension (which can cause CKD or more
commonly be a consequence of CKD)
o diabetes mellitus
o abnormal urinalyses
o problems with pregnancy (preeclampsia, early pregnancy loss)
• Careful drug history should be elicited.
o NSAIDs, COX-2 inhibitors, antimicrobials, chemotherapeutic
agents, antiretroviral agents, proton pump inhibitors,
phosphate-containing bowel cathartics, lithium.
• Evaluate uremic syndrome
o question about appetite, weight loss, nausea, hiccups,
peripheral edema, muscle cramps, pruritus, restless legs
• A family history of kidney disease + assessment of manifestations
in other organ systems (auditory, visual, integumentary) may lead
to the diagnosis of a heritable form of CKD (Alport or Fabry
disease, cystinosis) or shared environmental exposure to
nephrotoxic agents (heavy metals, aristolochic acid).
Physical Examination
• PE should focus on BP and target organ damage from hypertension.
• Funduscopy and Precordial examination should be carried out.
o Funduscopy – important in DM patient → may show evidence of • Reducing Intraglomerular Hypertension and Proteinuria
diabetic retinopathy, which is associated with nephropathy. o Control of systemic and glomerular hypertension is important
• Other PE manifestations of CKD: edema, sensory polyneuropathy.
• asterixis or a pericardial friction rub not attributable to other
causes usually signifies the presence of the uremic syndrome.
Laboratory Investigation {💻+📖}
• should focus on a search for clues to an underlying causative or
aggravating disease process and on the degree of renal damage
and its consequences.
• Serum and urine protein electrophoresis, looking for multiple
myeloma, should be obtained in all patients >35 years with
unexplained CKD
o especially if there is associated anemia and elevated, or even
inappropriately normal, serum calcium concentration in the face
of renal insufficiency.
• In the presence of glomerulonephritis, autoimmune diseases such
as lupus and underlying infectious etiologies such as hepa B and C
and HIV should be tested.
• Serum concentrations of calcium, phosphorus, vitamin D, and
PTH should be measured to evaluate metabolic bone disease.
• Evaluate hemoglobin concentration, iron, vitamin B12, folate
• A 24-h urine collection may be helpful, because protein excretion
>300 mg may be an indication for therapy with ACEi or ARBs.
Imaging Studies {💻+📖}
• The most useful imaging study is a renal ultrasound, which can
disease, the finding of bilaterally small kidneys supports the
diagnosis of CKD of long-standing duration.
• If the kidney size is normal, it is possible that the renal disease is
acute or subacute. The exceptions are:
o diabetic nephropathy (where kidney size is increased at the
onset of diabetic nephropathy before CKD supervenes)
o amyloidosis, and HIV nephropathy, where kidney size may be
normal in the face of CKD.
o Polycystic kidney disease that has reached some degree of
renal failure will almost always present with enlarged kidneys
with multiple cysts
• A discrepancy >1 cm in kidney length suggests either a
unilateral developmental abnormality or disease process or
renovascular disease with arterial insufficiency affecting one
kidney more than the other.
Kidney Biopsy {💻+📖}
• In the patient with bilaterally small kidneys, renal biopsy is not
advised because:
1 it is technically difficult and has a greater likelihood of causing
bleeding and other adverse con- sequences
2 there is usually so much scarring that the underlying disease
may not be apparent
3 the window of opportunity to render disease-specific therapy
has passed.
• Other contraindications to renal biopsy include:
o uncontrolled HTN, active UTI, bleeding diathesis (including
ongoing anticoagulation), severe obesity.
• Ultrasound-guided percutaneous biopsy – favored approach
o but a surgical or laparoscopic approach can be considered,
especially in the patient with a single kidney where direct
visualization and control of bleeding are crucial.
Treatment {💻+📖}
• Optimized glucose control in diabetes mellitus
• Immunomodulatory agent for glomerulonephritis
in slowing the progression of CKD. 125/ 75 mm Hg as the
target blood pressure in proteinuric CKD patients.
o ACE inhibitors and ARBS inhibit the angiotensin- induced
vasoconstriction of the efferent arterioles of the glomerular
microcirculation.
• Control of Blood Glucose
o 5.0-7.2 mmol/liter (90-130 mg/dl)
o Hemoglobin A1c <7 %
• Protein Restriction 0.60 and 0.75 g/kg per day
• Medication dose adjustment
o Avoid metformin, meperidine and oral hypoglycemic agent
eliminated by the kidney, NSAID
• Preparation for Renal Replacement Therapy
• Kidney Transplantation
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