CHRONIC KIDNEY DISEASE

Dr. SIVA THARSHINI

MD PSYCHIATRY
NHRIMH
03.03.2025 & 10.03.2025
CONTENTS
1. Definition
2. Classification of CKD
3. Clinical approach
4. Etiology
5. Pathophysiology
6. Clinical features
7. Investigations
8. Management
9. Homoeopathic management
CHRONIC KIDNEY DISEASE
♥ Previously termed chronic renal failure or insufficiency.
♥ CKD refers to a spectrum of longstanding (more than 3 months), usually progressive
processes associated with irreversible worsening of renal function and decline in
glomerular filtration rate (GFR).
♥ CKD spectrum ranges from abnormalities detectable only by laboratory testing to
uremia.
DEFINITION
 Glomerular filtration rate of <60 ml/min/1.73 m2 for 3 months or more, with or without
kidney damage or a urinary albumin to creatinine ratio > 65mg/mmol or protein
creatinine ratio of 100mg/ mol. [OR]
 Kidney damage for 3 or more months with or without decreased GFR, as evidenced
byany of the following:
▪ Microalbuminuria: Albumin excretion rate 30- 300 mg/ day in urine or urinary
albumin >30 mg/day excretion of creatinine.
▪ Macroalbuminuria: Albumin excretion rate in urine> 300 mg/ day
▪ Pathologic abnormalities such as abnormal findings on renal biopsy.
▪ Radiologic abnormalities such as scarring or polycystic kidneys on renal
ultrasound scan.
CLASSIFICATION OF CKD

CLINICAL APPROACH
♥ Duration of symptoms
♥ Drug intake: These include nonsteroidal anti-inflammatory agents, analgesic and other
medications (e.g. herbal medicines).
♥ Previous medical and surgical history, e.g. chemotherapy, SLE, malaria.
♥ Previous urinalysis or urea and creatinine values if performed.
♥ Family history of renal disease.
ETIOLOGY

PATHOPHYSIOLOGY
CLINICAL FEATURES
EDEMA
♥ In chronic glomerular disorders, development of intermittent edema and hematuria
indicates disease activity.
♥ Tubulointerstitial diseases- edema appears late.
HYPERTENSION
♥ Hypertension may appear early during the course of renal disease (90% in
glomerular and 30% in tubulointerstitial diseases).
♥ Rarely, uncontrolled hypertension can lead to precipitous and irreversible reduction
in GFR.
CARDIOVASCULAR MANIFESTATIONS
▪ Cardiovascular manifestations include left ventricular hypertrophy (LVH) due to
hypertension and anaemia, ischemic heart disease, congestive cardiac failure due to
fluid overload and myocardial dysfunction due to uremia (uremic cardiomyopathy).
▪ Electrolyte disturbances, particularly hyperkalemia can lead to bradycardia, syncope
and cardiac arrythmias.
▪ Other manifestations include premature atherosclerosis, vascular calcification due
to secondary hyperparathyroidism and pericarditis.
▪ CKD is a major risk factor for cardiovascular disease and even mild impairment of
renal function can lead to cardiovascular morbidity and mortality.
▪ Conversely, compromise in cardiac function worsens renal function too.
GASTROINTESTINAL MANIFESTATIONS
▪ The GI manifestations like anorexia, nausea, vomiting, dyspeptic symptoms,
constipation or diarrhea usually appear in Stage 4 CKD.
▪ Due to gastrointestinal mucosal ulcerations.
▪ Uremic stomatitis with dry mucous membranes, multiple small oral ulcers and parotitis
are seen in advanced uremia.
▪ ‘Uremic fetor’ describes the ammoniacal odor occurring in patients with advanced
renal failure and it is due to the hydrolysis of urea in saliva by bacterial urease.
▪ Severe abdominal pain and paralytic ileus may occur as a result of hypokalemia.
▪ Ascites may occur in advanced renal failure.
NEUROPSYCHIATRIC MANIFESTATIONS
▪ Paresthesias, sensory or motor peripheral neuropathy, pruritus, restless legs
syndrome and bladder dysfunction
▪ Subtle to gross behavioral abnormalities such as anxiety, depression, personality
changes and disturbances of sleep are the psychiatric manifestations.
▪ Flapping tremor (asterixis) and myoclonic jerks are features of uncontrolled uremia.
▪ Dialysis disequillibrium syndrome- When a patient is initiated on dialysis, abrupt and
rapid removal of urea from the blood may lead to higher concentration of urea in the
brain since it does not cross the blood-brain barrier rapidly. This leads to cerebral edema
and transient neuropsychiatric manifestations, collectively called DDS.
▪ This can be prevented by adjusting the initial few sessions of dialysis so as to achieve
very gradual fall in blood urea.
▪ Patients on long term dialysis may develop features of dementia and this is attributed
to aluminum intoxication which may occur due to intake of aluminum containing
antacids or through the water used for dialysis.
 ▪This is no longer a major problem at present because of water treatment which involves
removal of contaminants like aluminium in dialysis water and withdrawal of use of
aluminum hydroxide as a phosphate binder.
CUTANEOUS MANIFESTATIONS
▪ The characteristic sallow complexion in renal failure is due to pallor and the
deposition of yellowish brown urochrome pigment.
▪ Recurrent skin infections, dry scaly skin with severe itching, rashes, erythema, vesicles
and ulcerations are common.
▪ Pruritic hyperkeratotic papular eruptions or Kyrle’s disease occurs in diabetics.
▪ In stage V CKD, precipitation of urea on the surface of the skin gives rise to ‘uremic
frost’.
▪ Nail changes include pitting, burrowing and ‘half and half’ nails.
▪ In half and half nail, the distal half of the nail is pink or brown and the proximal half is
white or pale.
▪ The conjunctival deposition of calcium leads to redness and gritty feeling in the eye
also called the ‘uremic red eye’ while deposition of calcium as a band in the lamina
propria of the cornea leads to ‘band keratopathy.’
HEMATOLOGICAL MANIFESTATIONS
▪ Usually, the anemia is normocytic normochromic. The most important cause is
decreased secretion of erythropoietin (EPO). Other factors, apart from EPO deficiency
which contribute to renal anemia include the following.
 Circulating uremic toxins - bone marrow resistance to the effect of EPO.
 Reduced RBC survival (120 days to 80 days) probably due to mild
hemolysis.
 Platelet dysfunction - Bleeding, including occult gastrointestinal blood
loss.
 Iron deficiency.
 Hyperparathyroidism – bone marrow suppression or fibrosis.
 Folic acid deficiency.
 Chronic inflammation.
 Aluminum toxicity (rare).
▪ Prolonged anemia → worsening of renal function & left ventricular hypertrophy →
increased myocardial oxygen demand.
▪ Platelet dysfunction occurs due to factors like retention of uremic toxins, nitric oxide
and hyperparathyroidism.
SKELETAL ABNORMALITIES IN RENAL OSTEODYSTROPHY
❑ Renal osteodystrophy results from progressive kidney failure → hyperphosphatemia,
hypokalemia & secondary hyperparathyroidism.
❑ Disruptions in vitamin D metabolism and renal tubular defects contribute to
skeletal abnormalities.
❑ In children, growth retardation, bone deformities, and rickets occur due to uremic
toxins and hormone resistance.
❑ Non-uremic renal osteodystrophy can develop even before significant GFR reduction
due to renal tubular acidosis and vitamin D disturbances.
 ❑ Adults commonly present with high-turnover bone disease (osteitis fibrosa) caused by
hyperparathyroidism, characterized by subperiosteal bone resorption, "salt and
pepper" skull, vascular calcifications, and osteosclerosis.
❑ Severe cases may develop brown tumors or calciphylaxis, leading to painful skin ulcers
and gangrene.

RESPIRATORY MANIFESTATIONS
▪ Patients with advanced kidney disease may develop dyspnea due to pulmonary edema,
pleural effusion or severe metabolic acidosis.
▪ Flash pulmonary edema occurs in patients with renovascular diseases due to accelerated
hypertension.
▪ ‘Uremic lung’ may be seen radiologically as a butterfly shadow in the area of the hilum
and this is due to noncardiogenic pulmonary edema associated with increased
pulmonary capillary permeability and exudation of proteinaceous fluid into the alveoli.
▪ Uremic serositis may present as pleurisy with associated pleural friction rub or
underlying hemorrhagic pleural effusion.
INVESTIGATIONS- URINALYSIS
Physical examination: Fixed specific gravity around 1.010 (isosthenuria) is seen in CRF.
Chemical examination
❑ Hematuria may indicate glomerulonephritis.
❑ Proteinuria, if heavy, is strongly suggestive of glomerular disease.
 ❑ Glycosuria with normal blood glucose level is common in CRF.
Urine microscopy
❑ White cells in the urine usually indicate bacterial urinary infection, sterile pyuria
suggests papillary necrosis or renal tuberculosis.
❑ Eosinophils indicate allergic tubulointerstitial nephritis or cholesterol embolization.
❑ Red cells source may be from anywhere in the urinary tract between the glomerulus
and the urethral meatus.
❑ Red-cell casts are suggestive of glomerulonephritis.
❑ Granular casts indicate active renal disease.
❑ Broad casts are seen in CRF.
Urine culture should be performed. Early-morning urine samples should be cultured for
tuberculosis.
SERUM BIOCHEMISTRY
▪ Serum urea and creatinine: The most consistent abnormalities in CRF are elevated
levels of urea and creatinine. The level of serum creatinine correlates with the degree
of renal damage.
▪ Electrophoresis and immunofixation for myeloma.
▪ Extreme elevations of creatine kinase and a disproportionate elevation in serum
creatinine and potassium compared to urea suggestive of rhabdomyolysis.
▪ Other biochemical abnormalities include hypocalcemia, hyperphosphatemia,
hyperuricemia and hyperkalemia.
HEMATOLOGY
▪ Anemia
▪ Eosinophilia suggestive of allergic tubulointerstitial nephritis, vasculitis, or cholesterol
embolism.
▪ Peripheral smear with fragmented red cells (Burr cells) and/or thrombocytopenia
suggestive of intravascular hemolysis due to accelerated hypertension, hemolytic
uremic syndrome or thrombotic thrombocytopenic purpura.
▪ Markedly raised ESR is suggestive of myeloma.
IMMUNOLOGY
▪ Low complement components may be seen in active glomerular disease (e.g. SLE,
poststreptococcal glomerulonephritis).
▪ Autoantibody screening helpful autoimmune diseases (e.g. SLE).
▪ Antibodies to streptococcal antigens (ASOT, anti-DNase B) if post streptococcal
glomerulonephritis is suspected.
▪ Antibodies to hepatitis B and C
▪ Antibodies to HIV when HIV-associated renal disease is suspected.
▪ Malaria can cause glomerular disease in the tropics.
RADIOLOGICAL INVESTIGATION
▪ Ultrasound: Ultrasonography to assess the renal size and to exclude hydronephrosis.
Renal ultrasound usually shows shrunken kidneys in CRF. In diabetic
glomerulosclerosis, amyloidosis, polycystic kidney diseases, HIV nephropathy bilateral
hydronephrosis and myeloma, the kidneys may be of normal size.
▪ Plain abdominal radiography and CT (without contrast) to exclude low density renal
stones or nephrocalcinosis. CT may also useful for the diagnosis of retroperitoneal
fibrosis and useful in some patients with suspected obstructive nephropathy.
 ▪ Magnetic resonance angiography is useful in renovascular disease.

MANAGEMENT
▪ All patients require conservative management in the early stages.
▪ When the patient approaches Stage V CKD, renal replacement therapy has to be
introduced.
The general management consists of:
❑ Treatment of reversible causes of renal dysfunction.
❑ Preventing or slowing the progression of the renal disease.
❑ Treatment of the sequelae and complications of renal dysfunction.
❑ Identification of CKD stage and adequate preparation for renal replacement
therapy.
REVERSIBLE CAUSES OF RENAL DYSFUNCTION
☺ Relapse or flare of original renal disease eg. Crescentic transformation of primary
glomerulonephritis
☺ Decrease in renal perfusion eg. Hypotension, hemorrhage, drugs
☺ Infections eg. UTI, other infections
☺ Use of drugs which reduce GFR eg. NSAIDs, immunosuppressive drugs
☺ Nephrotoxic agents
☺ Urinary tract obstruction
☺ Accelerated hypertension
☺ Malnutrition, hypoalbuminemia, anemia
☺ Congestive cardiac failure, hepatic failure
☺ Persistent metabolic abnormalities such as hyperuricemia, hypercalcemia and
hypokalemia
PREVENTING OR SLOWING THE PROGRESSION OF DISEASE
▪ Control of hypertension and proteinuria: Goals of treatment include blood pressure
should be reduced < 0.3 g/24 hours. If creatinine is below 3 mg/dL, ACE inhibitors and
ARBs (inhibit the angiotensin-induced vasoconstriction of the efferent arterioles of the
glomerular microcirculation) are the drugs of choice.
▪ Diet
 ❑ Protein restriction to 0.60 and 0.75 g/kg per day, i.e. about 40 g/day (with higher
amount of essential amino acids). It reduces symptoms associated with uremia
and may also slow the rate of renal decline at earlier stages of renal disease.
❑ Avoid foods with high potassium.
❑ Salt restriction is necessary in most of the patients. However, patients with salt-
losing nephropathy (tubulo-interstitial disease) require a high-salt intake.
PREVENTING OR SLOWING THE PROGRESSION OF DISEASE
❑ Slowing progression of diabetic renal disease by control of blood glucose and
maintaining HbA1c in the range of 7.0 to 7.5.
❑ Use of lipid-lowering agents: Hypercholesterolemia is common in patients with
significant proteinuria, and in patients with CKD. Lipid lowering reduces vascular
events in non-dialysis CKD.
❑ Cessation of smoking.
❑ Exercise and weight reduction.
❑ Avoid nephrotoxic medications.
CORRECTIONS OF COMPLICATIONS
Treatment of hypocalcemia and hyperphosphatemia: Hypocalcemia:
o Treated with calcitriol or alphacalcidol (1-α-hydroxyvitamin D3) or paricalcitol
(19-nor 1,25-dihydroxyvitamin D3) and calcium supplementation.
o Serum calcium level should be monitored to avoid hypercalcemia. Oral calcium
carbonate also decreases the bioavailability of dietary phosphates.
Hyperphosphatemia: Treated with phosphate binders.
• Previously, aluminium hydroxide was used to bind phosphate in the gut and was
producing aluminium toxicity.
• Calcium carbonate and calcium acetate (serum calcium should be monitored).
• Polymer sevelamer carbonate (an anion-exchange resin).
• Lanthanum carbonate (a non-aluminum, non-calcium phosphate-binding agent)
has higher incidence of side effects.
Treatment of hyperparathyroidism:
▪ By the use of Calcium carbonate or acetate.
▪ Vitamin D analogues.
▪ Calcimimetics activate the calcium-sensing receptor in the parathyroid gland,
thereby inhibiting PTH secretion. Cinacalcet is used in patients who are on
dialysis.
MAINTENANCE FLUID AND ELECTROLYTE BALANCE
▪ Fluid retention: If there is evidence of fluid retention intake of dietary sodium is
restricted and loop diuretics may be necessary.
▪ Hyperkalemia: Usually responds to dietary restriction of potassium intake.
Occasionally, ion exchange resins may be necessary to remove potassium in the
gastrointestinal tract. If hyperkalemia occurs during diuretic therapy, reduce or stop
potassium-sparing diuretics, ACE inhibitors and ARBs.
▪ Acidosis: Sodium bicarbonate may be effective, but can cause edema and hypertension
owing to extracellular fluid expansion. Calcium carbonate, also used as a calcium
supplement and phosphate binder is useful in treating acidosis
TREATMENT OF ANEMIA IN CHRONIC RENAL FAILURE
❑ The anemia of erythropoietin (EPO) deficiency is treated with recombinant (synthetic)
human EPO (erythropoietin-alpha or -beta, or the longer-acting darbepoetin-alpha).
Administration of erythropoietin-alpha through subcutaneous route is contraindicated
in CRF and the intravenous route is used, initially 50 U/kg of epoetin-alpha over 1–5
min three times/week. EPO is less effective in the presence of iron deficiency, active
inflammation or malignancy, and in patients with aluminium overload (found in
dialysis).
❑ Blood pressure, hemoglobin concentration and reticulocyte count are measured every
2 weeks and the dose adjusted to maintain a target hemoglobin level of 10–12 g/dL.
❑ Hemoglobin >13 g/dL has been associated with increased incidence of cardiovascular
mortality.
❑ Specific treatment: Renal replacement therapy
IDENTIFICATION OF STAGE OF CKD & RRT
❑ The term RRT is used to describe the life support or saving modalities of treatment,
needed when the GFR falls below 15ml/min and generally resorted to, when it is less
than 5ml/min.
❑ Maintenance dialysis
❑ Kidney transplantation

HOMOEOPATHIC MANAGEMENT
REPERTORIAL APPROACH
BOGER’S REPERTORY
❑ Sensation and complaint in general : Uremia
❑ Urine: Albuminous
❑ Urine : Flocculent and filamentous
❑ Urine : Turbid, cloudy
BOERICKE’S REPERTORY
❑ Generalities: Kidney disease from
 ❑ Urinary system; Kidney: Acute and sub acute parenchymatous nephritis;
concomitants; uremic symptoms
❑ Kidney: Uremia
BOERICKE’S REPERTORY
❑ Kidney: Uremia: convulsions
❑ Kidney: Uremia: headache
❑ Kidney: Uremia: vomiting
SYNTHESIS REPERTORY
❑ Generals: Uremia
❑ Kidney: Pain
❑ Kidney: Suppression of urine; convulsions with
❑ Urine: Casts, containing
HOMOEOPATHIC THERAPEUTICS
 AMMONIUM CARB
Heaviness in all organs, swelling of glands, acid reactions; prostration; frequent desire to
urinate with tenesmus; urine white, scanty, bloody copious turbid and fetid.
 ARSENIC ALB
Urine is scanty, burning involuntary. Bladder as if paralyzed. Albuminuria. Nephritis.
Uremia. Atony of bladder in old persons. Epithelial cells cylindrical clots of fibrin and
globules of pus and blood. Feeling of weakness in abdomen after urination. Retention of
urine, as if the bladder were paralyzed after childbirth. Urine black as if mixed with dung.
Dysuria.
 AURUM MET
Painful retention of urine, with urgent inclination to make water, and pressure on the
bladder. Frequent emission of watery urine. Urine turbid, like buttermilk, with thick mucus-
like sediment.
 OPIUM
Scanty, deep coloured (dark brown) urine, with sediment like brick dust. Retention of urine.
Coma. Insomnia. Intermittent respiration.
 PHOSPHORUS
Urine turbid, brown, with red sediment. Uremia with acute atrophy of brain.
 PICRIC ACID
Complete anuria, nephritis with profound weakness.
 PLATINA
Red urine with a white cloud, or else which becomes turbid, and deposits red sediment.
Slow but frequent emission of urine.
 TEREBINTHINA
Pressure in the kidneys when sitting, going off during motion. Sensation of heaviness and
pain in region of kidneys. Transient movement in region of bladder during stool as if
bladder were suddenly distended and bent forward. Frequent desire to urinate. Violent
burning drawing pain in region of kidneys. Spasms from any attempt to urinate. Suppressed
secretion of urine. Urine smelling strongly of violets; deposit of mucus, or thick, muddy
deposit. Thick, slimy, yellowish white sediment in urine. Much blood with very little urine
and constant painful Dysuria. Burning sensation, incisive pains, and spasmodic tenesmus
of bladder.