Nephritis refers to inflammation of the kidneys that can be caused by various factors like infection, autoimmune disease, or kidney disease. It affects the glomeruli, tubules, or surrounding tissue and can lead to impaired kidney function. Symptoms vary depending on the specific type and cause of nephritis but may include blood or protein in the urine, high blood pressure, swelling, and changes in kidney function test results. Treatment involves addressing the underlying cause, managing complications, and potentially using medications, dietary changes, or dialysis.

2. Nephritis: Inflammation of the
kidney, which causes impaired
kidney function. Nephritis can be
due to a variety of causes,
including kidney
disease, autoimmune disease ,
and infection. Treatment depends
on the cause.

3. Nephritis is inflammation of
the kidneys and may involve
the glomeruli, tubules,
or interstitial tissue surrounding the
glomeruli and tubules
Nephritis refers to a medical
condition characterized by an
inflammation of the kidneys.
Glomerulonephritis is an inflammation
of the glomerular capillaries.

4.  overall prevalence was 4.4 per
100,000 population
 7.1 per 100,000 in women,
 1.4 per 100,000 in men.

5. There are different types of nephritis. Each type is based
on the part of the kidney that has been affected with the
condition. The three main areas commonly affected are the
glomeruli, tubule, and interstitial renal tissue.
Glomerulonephritis
Pyelonephritis
Interstitial Nephritis

6. This condition refers to the
inflammation of the tiny
capillaries in the kidneys called
glomeruli, which task is to filter
blood. When they become
inflamed, they are unable to
effectively filter the blood

7. Glomerulonephritis is
inflammation of the
tiny filters of kidneys
(glomeruli).

8.  Infections
 Post-streptococcal glomerulonephritis.
Glomerulonephritis may develop a week or two after recovery
from a strep throat infection or, rarely, a skin infection (impetigo). To fight
the infection, your body produces extra antibodies that can eventually
settle in the glomeruli, causing inflammation.
Children are more likely to develop post-streptococcal
glomerulonephritis than are adults, and they're also more likely to recover
quickly.
 Bacterial endocarditis.
Bacteria occasionally can spread through your bloodstream
and lodge in your heart, causing an infection of one or more of your
heart valves. You're at greater risk of this condition if you have a
heart defect, such as a damaged or artificial heart valve. Bacterial
endocarditis is associated with glomerular disease, but the
connection between the two is unclear.
 Viral infections.
Viral infections, such as the human immunodeficiency virus
(HIV), hepatitis B and hepatitis C, can trigger glomerulonephritis

9.  Vasculitis
Polyarteritis.
This form of vasculitis affects small and medium blood vessels in many
parts of your body, such as your heart, kidneys and intestines.
Granulomatosis with polyangiitis.
This form of vasculitis, formerly known as Wegener's granulomatosis,
affects small and medium blood vessels in your lungs, upper airways and kidneys.
 Immune Response
Lupus
A chronic inflammatory disease, lupus can affect many parts of your body, including
your skin, joints, kidneys, blood cells, heart and lungs.
Goodpasture's syndrome
A rare immunological lung disorder that can mimic pneumonia, Goodpasture's
syndrome causes bleeding in your lungs as well as glomerulonephritis.
IgA nephropathy
Characterized by recurrent episodes of blood in the urine, this primary glomerular
disease results from deposits of immunoglobulin A (IgA) in the
glomeruli. IgA nephropathy can progress for years with no noticeable symptoms
 Risk factors :
HTN-Diabetic Nephropathy - Focal segmental Glomerulo sclerosis

10. Acute glomerulonephritis
Primarily a disease of children older than 2 years of age, but it
can occur at nearly any age
Chronic glomerulonephritis:
One of a group of kidney diseases characterized by long-
term inflammation and scarring of
the glomeruli (microscopic structures in the kidney that
filter blood and produce urine). This form of kidney
disease usually develops slowly (over years) and may not
produce symptoms at the outset. When symptoms and
signs do appear, they typically include blood in the urine
(hematuria), swelling (edema), high blood pressure, foamy
urine (due to protein content), and frequent nighttime
urination.

12.  The primary presenting feature
:Hematuria, which may be
microscopic identifiable
 through microscopic: examination or
(visible to the eye)
 cola- colored Urine because of RBCs
and protein plugs or casts. (RBC casts
indicate glomerular injury.)
 Oliguria : Patient has acute renal
failure
 Elevated BUN and serum creatinine levels
 feet are slightly swollen at night
 Loss of weight and strength
 increasing irritability
 Increased need to urinate at night
(nocturia).
 Headaches,
 Dizziness
 Digestive disturbances
 Blood pressure may be normal or severely
elevated.
 Retinalfindings include hemorrhage,
exudate, narrowed tortuous arterioles, and
papilledema.
 Mucous membranes are pale because of
anemia.
 Cardiomegaly, a gallop rhythm, distended
neck veins,
 Crackles can be heard in the lungs

13.  Fewer
 Chills
 Nausea
 Headache
 Flank pain
 Cloudy urine
 Foul smell – urine
Azotemia
Pyuria
Anemia
Acidosis
Proteinuria
Cerebral symptoms. Cerebral symptoms
consisting mainly of headache,
drowsiness, convulsions, and vomiting
occur in connection with hypertension in a
few cases.

14.  HISTORY TAKING
 PHYSICAL EXAMINATION
 BLOOD TEST :
 creatinine Elevated
 blood urea nitrogen Elevated
 Hyperkalemia due to decreased potassium
excretion, acidosis, catabolism, and excessive
potassium intake from food and medications
 ABG :Metabolic acidosis from decreased acid
secretion by the kidney and inability to
regenerate bicarbonate
 Anemia secondary to decreased erythropoiesis
(production of RBCs)
 Hypoalbuminemia with edema secondary to
protein loss through the damaged glomerular
membrane
 Increased serum phosphorus & magnesium
level due to decreased renal excretion of
phosphorus & Mg
 Decreased serum calcium level (calcium binds
to phosphorus to compensate for elevated
serum phosphorus levels)
 Impaired nerve conduction due to electrolyte
abnormalities and uremia
 KIDNEY BIOPSY PROCEDURE
 URINE TEST.
 might show red
blood cells and red
cell casts in your
urine, an indicator of
possible damage to
the glomeruli.
 white blood cells, a
common indicator of
infection or
inflammation,
 Increased protein,
which can indicate
nephron damage.
 Other indicators,
such as increased
blood levels of
creatinine or urea,
are red flags.
 Imaging tests.
kidney X-ray, an
ultrasound exam or a CT
scan

15. Goal
 Preserve kidney function
 Treating complications promptly

16. Dietary protein is restricted when renal insufficiency and nitrogen retention
(elevated BUN) develop.
Sodium is restricted when the patient has hypertension, edema, and heart
failure.
Loop diuretic medications and antihypertensive agents may be prescribed to
control hypertension. Prolonged bed rest has little value and does not alter
long-term outcomes.
Weight is monitored daily
Initiation of dialysis is considered early in the course of the disease to keep
the patient in optimal physical condition, prevent fluid and electrolyte
imbalances, and minimize the risk of complications of renal failure

17. Pharmacological management
 Antibiotic therapy to prevent streptococcal
infection ( Prophylaxis ).
 Steroids to suppress immunity.
 Corticosteroids. These strong anti-inflammatory drugs can
decrease inflammation
 Immunosuppressive drugs. These drugs, which are related to the
ones used to treat cancer or prevent the rejection of transplanted
organs, work by suppressing immune system activity that
damages the kidneys. They
include cyclophosphamide (Cytoxan), azathioprine (Imuran) and
mycophenolate (Cellcept)
 Medications to prevent blood clots or lower blood pressure if
needed
Dialysis

18. Pyelonephritis is inflammation
of renal pelvis and parenchyma
caused by a bacterial infection

19.  Renal calculi
 Malignancy
 Hydro nephrosis
 Trauma
 Urinary tract infection
 E. Coli

20.  Acute
 Chronic

22.  Fewer
 Chills
 Nausea
 Headache
 Flank pain
 Cloudy urine
 Foul smell – urine
Azotemia
Pyuria
Anemia
Acidosis
Proteinuria

23.  HISTORY TAKING
 PHYSICAL EXAMINATION
 BLOOD TEST :
 creatinine Elevated
 blood urea nitrogen Elevated
 Hyperkalemia due to decreased potassium
excretion, acidosis, catabolism, and excessive
potassium intake from food and medications
 ABG :Metabolic acidosis from decreased acid
secretion by the kidney and inability to
regenerate bicarbonate
 Anemia secondary to decreased erythropoiesis
(production of RBCs)
 Hypoalbuminemia with edema secondary to
protein loss through the damaged glomerular
membrane
 Increased serum phosphorus & magnesium
level due to decreased renal excretion of
phosphorus & Mg
 Decreased serum calcium level (calcium binds
to phosphorus to compensate for elevated
serum phosphorus levels)
 Impaired nerve conduction due to electrolyte
abnormalities and uremia
 KIDNEY BIOPSY PROCEDURE
 URINE TEST.
 might show red
blood cells and red
cell casts in your
urine, an indicator of
possible damage to
the glomeruli.
 white blood cells, a
common indicator of
infection or
inflammation,
 Increased protein,
which can indicate
nephron damage.
 Other indicators,
such as increased
blood levels of
creatinine or urea,
are red flags.
 Imaging tests.
kidney X-ray, an
ultrasound exam or a CT
scan

24. Goal
 Preserve kidney function
 Treating complications promptly

25. Dietary protein is restricted when renal insufficiency and nitrogen retention
(elevated BUN) develop.
Sodium is restricted when the patient has hypertension, edema, and heart
failure.
Loop diuretic medications and antihypertensive agents may be prescribed to
control hypertension. Prolonged bed rest has little value and does not alter
long-term outcomes.
Weight is monitored daily
Initiation of dialysis is considered early in the course of the disease to keep
the patient in optimal physical condition, prevent fluid and electrolyte
imbalances, and minimize the risk of complications of renal failure

26. Pharmacological management
 Antibiotic therapy : sulphonamide
 Steroids to suppress immunity.
 Analgesics
 Corticosteroids. These strong anti-inflammatory drugs can
decrease inflammation
 Immunosuppressive drugs. These drugs, which are related to the
ones used to treat cancer or prevent the rejection of transplanted
organs, work by suppressing immune system activity that
damages the kidneys. They
include cyclophosphamide (Cytoxan), azathioprine (Imuran) and
mycophenolate (Cellcept)
 Medications to prevent blood clots or lower blood pressure if
needed
Dialysis

28. It is a kidney
disorder , in which
there is an
inflammation of
interstitial space of
renal tubules

29.  Infections.
 Autoimmune disorders, such as Kawasaki disease or
Sjogren syndrome.
 A reaction to a medicine, such as certain antibiotics.
 Too much of certain medicines. These include
diuretics (water pills) or pain relievers, such as
acetaminophen, aspirin, or a non-steroidal anti-
inflammatory drug (NSAID).
 Unbalanced levels of certain nutrients in your blood.
This includes too little potassium or too much
calcium.

32.  The primary presenting feature
:Hematuria, which may be
microscopic identifiable
 through microscopic: examination or
(visible to the eye)
 cola- colored Urine because of RBCs
and protein plugs or casts. (RBC casts
indicate glomerular injury.)
 Oliguria : Patient has acute renal
failure
 Elevated BUN and serum creatinine levels
 feet are slightly swollen at night
 Loss of weight and strength
 increasing irritability
 Increased need to urinate at night
(nocturia).
 Headaches,
 Dizziness
 Digestive disturbances
 Blood pressure may be normal or severely
elevated.
 Retinalfindings include hemorrhage,
exudate, narrowed tortuous arterioles, and
papilledema.
 Mucous membranes are pale because of
anemia.
 Cardiomegaly, a gallop rhythm, distended
neck veins,
 Crackles can be heard in the lungs

33.  Fewer
 Chills
 Nausea
 Headache
 Flank pain
 Cloudy urine
 Foul smell – urine

Azotemia
Pyuria
Anemia
Acidosis
Proteinuria

34.  HISTORY TAKING
 PHYSICAL EXAMINATION
 BLOOD TEST :
 creatinine Elevated
 blood urea nitrogen Elevated
 Hyperkalemia due to decreased potassium
excretion, acidosis, catabolism, and excessive
potassium intake from food and medications
 ABG :Metabolic acidosis from decreased acid
secretion by the kidney and inability to
regenerate bicarbonate
 Anemia secondary to decreased erythropoiesis
(production of RBCs)
 Hypoalbuminemia with edema secondary to
protein loss through the damaged glomerular
membrane
 Increased serum phosphorus & magnesium
level due to decreased renal excretion of
phosphorus & Mg
 Decreased serum calcium level (calcium binds
to phosphorus to compensate for elevated
serum phosphorus levels)
 Impaired nerve conduction due to electrolyte
abnormalities and uremia
 KIDNEY BIOPSY PROCEDURE
 URINE TEST.
 might show red
blood cells and red
cell casts in your
urine, an indicator of
possible damage to
the glomeruli.
 white blood cells, a
common indicator of
infection or
inflammation,
 Increased protein,
which can indicate
nephron damage.
 Other indicators,
such as increased
blood levels of
creatinine or urea,
are red flags.
 Imaging tests.
kidney X-ray, an
ultrasound exam or a CT
scan

35. Goal
 Preserve kidney function
 Treating complications promptly

36. Dietary protein is restricted when renal insufficiency and nitrogen retention
(elevated BUN) develop.
Sodium is restricted when the patient has hypertension, edema, and heart
failure.
Loop diuretic medications and antihypertensive agents may be prescribed to
control hypertension. Prolonged bed rest has little value and does not alter
long-term outcomes.
Weight is monitored daily
Initiation of dialysis is considered early in the course of the disease to keep
the patient in optimal physical condition, prevent fluid and electrolyte
imbalances, and minimize the risk of complications of renal failure

37. Pharmacological management
 Antibiotic therapy : sulphonamide
 Steroids to suppress immunity.
 Analgesics
 Corticosteroids. These strong anti-inflammatory drugs can
decrease inflammation- CONTRA INDICATED IN DRUG
INDUCED
 Immunosuppressive drugs. These drugs, which are related to the
ones used to treat cancer or prevent the rejection of transplanted
organs, work by suppressing immune system activity that
damages the kidneys. They
include cyclophosphamide (Cytoxan), azathioprine (Imuran) and
mycophenolate (Cellcept)
 Medications to prevent blood clots or lower blood pressure if
needed
Dialysis

39.  Ineffective breathing pattern related to the inflammatory process.
 Altered urinary elimination related to decreased bladder capacity
or irritation secondary to infection.
 Excess fluid volume related to a decrease in regulatory
mechanisms (renal failure) with the potential of water.
 Risk for infection related to a decrease in the immunological
defense.
 Imbalanced nutrition less than body requirements related
to anorexia, nausea, vomiting.
 Risk for impaired skin integrity related to edema and pruritus.
 Hyperthermia related to the ineffectiveness of thermoregulation
secondary to infection.

41. The prognosis is poor. At least 80% of people
who are not treated develop end-stage kidney
failure within 6 months. The prognosis is
better for people younger than 60 years

42.  Renal failure
 Encephalopathy,
 Heart failure
 Pulmonary
edema

44. BOOK REFERENCES
1. BASVANTHAPPA, MEDICAL SURGICAL NURSING, 2NDEDITION, JAYPEE
PUBLISHERS,NEW DELHI
2. BRUNNER AND SUDDARTHS, TEXT BOOK OF MEDICAL SURGICAL NURSING,
11NTHEDITION, LIPPINCOTT WILLIAMS AND WILKINS, WOLTER KLUWER (INDIA)
PVT LTD,2008
3. DANIIEL RICK et-al, CONTEMPARARY MEDICAL SURGICAL NURSING, 2NDEDITION
2007, SWAT PRINTERS,
4. DONNA D Et-al, MEDICAL SURGICAL NURSING, 2ndEDITION WB SAUNDERS COMPANY

45. 5. ELIZEBATH A MARTIN Et-al
MINI DICTIONARY FOR NURSES, OXFORD UNIVERSITY PRESS.
6. JAYA KURUVILA, ESSENTIALS OF CRITICAL CARE NURSING, JAYPEE BROTHERS
MEDICAL PUBLISHERS PVT LTD, NEWDELHI , 2007.
7. JOYCE M BLACK, Et-all, MEDICAL SURGICAL NURSING,CLINICAL MANAGEMENT
FOR POSITIVE OUTCOMES, 8THEDITION,ELSAVIER INDIA PVT LTD, 2010.
8. MOSBY, 2006 DRUG CONSULT FOR NURSES, ELSAVIER PUBLICATIONS 2006.
9. NANCY HOLMES Et-al, MASTERING MEDICAL SURGICAL NURSING DISORDERS &
TREATMENT & NURSING TIPS ANDGUIDELINES PATIENT TEACHING AND OUT COME,
SPRINGHOUSE .
10. SANDRA N NETTINA, THE LIPPINCOTT MANUAL OF NURSING PRACTICE, 7NTH
EDITION, LIPPINCOTT PUBLISHERS, PHILADELPHIA, 2003.