Nephritis: Causes, Symptoms, and Treatment

This article provides an overview of nephritis, a non-infectious inflammation of the kidney. It discusses the causes, symptoms, and treatment options for nephritis, including diagnostic methods and management strategies. The article also explores the pathophysiology of nephritis and identifies predisposing factors. Additionally, it highlights the signs and symptoms of nephritis and discusses the stress response and hemodynamics associated with this condition.

Running head: HEALTH
Student name
Student No.
Unit
Title: Nephritis

HEALTH
Nephritis is a non-infectious inflammation that affects the glomerulus, interstitium
and the tubules of the kidney parenchyma. The inflammation of the glomerulus is known as
the glomerulonephritis while that of the interstitium and the tubules is the tubulointerstitial
nephritis. According to Sandys et al. (2018), glomerulonephritis is more popular and most
people would think of glomerular infection when nephritis is mentioned. The nephritic
syndrome is characterized by proteinuria, oliguria, uremia, red blood cells present in urine,
hematuria and hypertension. Proteinuria and hematuria alone suggest glomerular
inflammation. Stephens (2018) claims there are three types of nephritis. They include
interstitial nephritis, pyelonephritis and glomerulonephritis. Interstitial nephritis is
characterized by inflammation of the space between the kidney tubules causing the swelling
of the kidney. Pyelonephritis is caused by bacterial infection. The bacteria causes the kidney
to swell. The infection stars at the bladder, moves up through the ureter then to the kidneys.
Stephens describes glomerulonephritis just like Sandys and his colleagues describe it, that it
is the inflammation of glomeruli. This inflammation impairs the process of blood filtration.
Diagnosis
A patient showing high levels of serum creatinine and white blood cells and red blood
cells in urine or eosinophiluria should be suspected of nephritis. For the drug induced
nephritis, it should be noticed after the onset of laboratory findings on the initiation of the
drug thought to cause nephritis (Praga and Appel, 2018). It is unnecessary to carry out
definitive diagnosis to some patients such as those who show sudden improvement after
stopping the drug causing nephritis. Therefore, renal biopsy is recommended for these
patients. This kidney biopsy is carried out to the following patients: patients whose urinalysis
test shows presence of nephritis but have not been prescribed to any drug thought to cause
nephritis; patients using drugs that may cause nephritis but have no characteristic urinalysis;
patients under treatment for nephritis using glucocorticoids; patients showing advanced renal

HEALTH
failure, patients showing features that make diagnosis of nephritis uncertain; and lastly
patients with assumed drug related nephritis, not initially prescribed with glucocorticoids and
do not show recovery after stoppage of drug therapy (Praga and Appel, 2018). In this case,
the health professionals gives the patient some time before carrying out the renal biopsy.
Kidney biopsy may also be considered for patients showing characteristic urinalysis but no
elevated creatinine. These patients are rarely noticed because urinalysis is carried out after
detecting rise in serum creatinine.
According to Irastorza et al. (2012), renal biopsy is mandatory for patients with lupus
nephritis. Renal biopsy should be used as a preferential procedure depending on how severe
the patient’s condition is. For systematic lupus erythematous (SLE) to be present, the test
must show rise in creatinine, haematuria, proteinuria, reduced rate of glomerular filtration
and active urinary sentiments. Results showing haematuria should be carefully interpreted as
it could be as a result of vaginal contamination, tumours, familial haematuria or even
infection of the urine. The presence of glomerulonephritis is indicated by abnormal routine
urinalysis (Mayo clinic, 2018). The following tests are carried out to diagnose
glomerulonephritis: urine test- presence of red blood cells and red cell cast in the urine
indicate a possibility of damaged glomeruli. Urinalysis may also show red blood cells which
indicates inflammation or an infection and high levels of protein, which is an indicator of
nephron damage. Blood test- by measuring the levels of wastes such as blood urea, nitrogen
and creatinine, this test could indicate the level of kidney damage and glomeruli impairment
(Russo et al. 2014). Imaging test- after detecting evidence of kidney damage, the health
professional may recommend studies carried out to visualize the kidneys. These tests could
be CT scan, ultrasound examination or even kidney x-ray. Kidney biopsy- this is carried out
to determine the cause of the kidney inflammation. According to Mok (2012), urine

HEALTH
eosinophil, imaging studies and renal biopsy are the diagnostic methods used to identify
interstitial nephritis.
Pathophysiology
The rate of renal blood flow is about 40ml/100g of tissue in a minute, which is much
greater as compared to the blood flowing into other vascular beds such as the heart and liver.
This exposes the renal tissues to harmful agents circulating in the blood. Glomerular filtration
depends on high intra and transglomerular pressure making the glomerular capillaries
vulnerable to hemodynamic injuries. For this case Couser and Johnson (2014) classified
glomerular hypertension and hyperfiltration as the leading cause of renal infections. They
further claim that the main causes of renal injury are as a result of immunological reactions,
tissue ischaemia and hypoxia, endogenous substances, exogenic agents, and genetic factors.
Genetic defects account factors account for the least cause of nephritis. The hereditary
nephritis is transmitted as an X-linked dominant trait, whereby mutation of the COL4A5 gene
encodes the α5 chain of type IV collagen found on the X chromosome. Metabolic,
hemodynamic and toxic substances may also lead to glomerular impairment. Jeloka (2012)
think that tubulointerstitial injury is caused by impairment of the interstitium and the tubules.
Excess reabsorption of proteins in the proximal tubule could cause lysosomal rapture
hence direct tubular toxicity. In children, nephritis is thought to be as a result of autoimmune
response which are modified by genetic factors. This activates some biological processes
leading to glomerular inflammation (Niaudet, 2018). According to Mayo Clinic (2018),
glomerulonephritis could be as a result of recovery of strep through infection or impetigo.
During the process of recovery, the body produces excess antibodies, which after settling at
the glomeruli cause inflammation. Researchers claim there is a connection between bacterial

HEALTH
endocarditis and nephritis, though their relation is unclear. Nephritis could also be caused by
immune diseases such as lupus, which is chronic inflammatory infection of the body; good
pasture’s syndrome, a lung disorder that mimics pneumonia and IgA nephropathy,
characterized by traces of blood in urine.
Predisposing factors
According to Buyon et al. (2017), out of 3 adult in the US, one is at risk of contracting
a kidney disease. Most kidney infections are caused by high blood pressure and diabetes.
Other risk factors include family history- whereby knowing ones family history helps take
protective measures, age-being above 60 increases the risk of contracting kidney infections;
race or ethnicity, with African Americans, Asian Americans, Hispanics and Native
Americans being at a higher risk. Among these people, African-American are at a higher risk
of kidney failure (McInerny et al. 2017). This is because the African-Americans are more
prone to diabetes which contributes to kidney infections. Hispanics are two times more likely
to suffer from nephritis as compared to the whites. This attributed to the high blood pressure
cases among the Hispanians. Smoking is thought to the concentration of albumin in urine.
The amount of urinary albumin excreted is proportional to the amount of cigarettes smoked.
Studies have shown that smoking is a renal risk factor as it put the patient at a risk of diabetic
nephropathy for diabetic patients. Further research has shown smoking leads to high blood
pressure and structural alteration of the kidney (Cha et al. 2015). For IgA nephropathy
patients, smoking increases the level of serum creatinine. Obesity is a risk factor for
cardiovascular infections. It is therefore a risk factor for nephritis as CVDs are risk factors
too.

HEALTH
Signs and Symptoms
For lupus nephritis, swelling of legs, feet and ankles and sometimes hands and face
are the first noticeable symptoms. High blood pressure, dark urine, weigh gain and frothy
urine could also be noticed (Stephens, 2018). According to Mayo Clinic (2018), the signs and
symptoms of glomerulonephritis are dependent on the cause and whether the disease is acute
or chronic. The signs and symptoms of glomerulonephritis include pink colored urine, foamy
urine due to protein present in the urine (proteinuria), high blood pressure, red blood cells in
urine and fluid retention, which lead to swelling of hands, feet, face and the abdomen. For
nephrotic syndrome, the signs and symptoms include edema (swelling of eyes and feet),
fatigue, foamy urine due to excess protein in the urine. loss of appetite and weight gain as a
result of excess fluid retention (Mayo Clinic, 2018).
Treatment
Treatment of nephritis depends on the conditions causing the disease. Stephens (2018)
claims that antibiotic are the typical prescriptions for nephritis. For serious nephritis
infection, intravenous IV antibiotics are administered. These antibiotics work faster than
those in pill form. One treatment of nephritis is controlling high blood pressure especially
when the disease is due to hypertension. This could face some challenges especially when the
kidneys are not functioning well. The patient is prescribed with blood pressure medication
such as angiotensin converting enzyme inhibitors. These could include captopril, lisinopril
and Aceon. Angiotensin receptor blockers such as losartan, Avapro and Diovan could be
administered to the patient. Corticosteroids help reduce immune response and are prescribed
when the patient’s immune system seems to fight against the kidneys. Health care
practitioners in other cases would use plasmapheresis method in reducing immune triggered
inflammations. This method involves removal of plasma then replacing it with donated

HEALTH
antibodies free plasma or intravenous fluid (Floege and Amann, 2016). For chronic
glomerulonephritis, it is recommended that the patient reduced the levels of salt, potassium
and protein in their diet. Calcium supplements are prescribed with regulated intake of fluids.
One could also be advised to take diuretics to reduce swelling. In advanced cases (kidney
failure), kidney dialysis is carried out. In other cases kidney transplant could be the only
option.
Parikh and Rovin (2016) claim that lupus nephritis was treated using induction and
mainstream approaches. Induction aims at rapidly attenuating renal inflammation to allow the
infected renal parenchyma to heal. Other than the use of cyclophosphamide and prednisone
for induction, a research by the National Institute of Health revealed that the use of
cyclophosphamide and corticosteroids reduced kidney lapses and cases of kidney failure. In
cases of the disease is severe, high dose intravenous methylprednisolone is administered
about 3 days with oral corticosteroids. In case nephritis is as a result of diabetes, metoprolol
succinate could be used (Farkner and Kushner, 2008). Metopolol succinate has different side
effects on the patient. These could include abnormal low blood pressure, dizziness,
depression, body salts imbalance and slow heartbeat. Mayo clinic (2018) think there could be
no ways to prevent nephritis. However, they recommend prompt treatment of strep infection,
prevent any infection that could lead to nephritis and control blood sugar levels and high
blood pressure.
Stress response
Patients undergoing dialysis on chronic renal failure face both socio-economic and
psychological problems. These problems are mostly stress as a result of change in social
relationships, financial difficulties, restricted leisure, lack of holiday vacations, fear of death
or disability, dependence on artificial kidney machine, physical fatigue, inability to predict

HEALTH
their future and change in marital relationship also. These patients are limited on their fluid
intake as they should not consume more than 500ml a day. This also adds on their stress
(Assadi, 2013). These patients are restricted to a certain diet, which also psychologically
affects them. Patients diagnosed with glomerulonephritis are at a higher risk of contracting
cardiovascular infections. According to Hutton et al. (2017), previous researches have not
given a clear relationship between cardiovascular diseases and nephritis and whether the high
risk of cardiovascular diseases in nephritis is attributed to the disease itself or concurrent
cardiovascular risk factors. However, patients with nephritis are at a high risk of suffering
from CVD and cardiovascular deaths.
Voss et al (2015) claim that any stage of renal infection is accompanied with
significant gastrointestinal symptoms. Similarly, patient suffering from GI can also show
significant nephritis complications. Patients at the advanced stages of renal infections are at a
higher risk of GI infections. Among the many changes associated with chronic kidney disease
is the complex metabolic acidosis. Nephritis influences the normal functioning of the kidney,
therefore increasing the acid retention hence causing a lot of deleterious consequences like
protein energy wasting. Metabolic acidosis has also been associated with kidney damage and
increased progression of chronic kidney damage through mechanism designed to promote
acid excretion (Kovesdy, 2012).
Hemodynamics
The kidney is the body organ responsible for maintaining the body fluid homeostasis
by maintaining water, electrolytic and acid base balance, excretion of uremic toxins and it is
responsible for producing some hormones like renin (Tojo and Kinugasa, 2012). In the
current days, drugs are among the leading causes nephritis. Drugs induce their toxic effects
by pathogenic mechanisms. Drug induced nephritis is characterized by reduced rates of

HEALTH
glomerular filtration (Naughton 2008). Glomerulonephritis, which affects the glomerulus,
makes it unable to carry out its filtration functions. Carbon monoxide gas affects the central
nervous system. This could result to renal failure due to hypoxia and rhabdomyolysis.
According to Csongradi, Juncos, Drummond, Vera and Stec (2012) carbon monoxide is
produced by heme oxygenese which is released to the kidneys in response to different
pathological and physiological stimuli. Studies show that carbon monoxide helps limit
oxidative injuries, promote cell survival and reduce cell apoptosis.
Oxygenation
Renal oxygenation is the balance between the oxygen supply and its consumption in
the renal tissues. Under normal conditions, the oxygen supply should exceed the oxygen
demand to the renal tissues. In case of nephritis, this balance is disturbed. This leads to
oxidative stress which in turn affects electrolytic active transport efficiency. The reduced
efficiency of electrolytic transport is attributed to different mechanisms like alteration of
electrolytic permeability and effects on sodium or potassium ions (Hansell, Welch,Blantz and
Palm, 2013). Friederich-Persson et al (2013) think that the kidneys do not show any
relationship between oxygen demand and supply. Increasing renal blood flow increases the
tubular electrolytic load by increasing the glomerular filtration. Renal active transport
therefore increases and the kidney demands more energy. This results to increased oxygen
consumption in the kidneys and nephropathy develops. Kidney diseases could be associate to
chronic lung diseases. Hypoxia results when the kidney receives insufficient blood which
could lead to chronic renal disease. The kidney becomes full of fibrous tissue and blood
filtration and regulation of salts is impaired.

HEALTH
References
Assadi F. (2013). Psychological impact of chronic kidney disease among children and
adolescents: Not rare and not benign. Journal of nephropathology, 2(1), 1-3. Doi:
10.5812/nephropathol.8968
Buyon, J. P., Kim, M. Y., Guerra, M. M., Lu, S., Reeves, E., Petri, M., Laskin, C. A.,
Lockshin, M. D., Sammaritano, L. R., Branch, D. W., Porter, T. F., Sawitzke, A.,
Merrill, J. T., Stephenson, M. D., Cohn, E. and Salmon, J. E. (2017). Kidney
Outcomes and Risk Factors for Nephritis (Flare/De Novo) in a Multiethnic Cohort of
Pregnant Patients with Lupus. Clin J Am Soc Nephrol. Vol. 12, No. 6. Doi:
10.2215/CJN.11431116
Cha, Y. J., Lim, B. J., Kim, B. S., Kim, Y., Yoo, T. H., Han, S. H., Kang, S. W., Choi, K. H.,
Jeong, H. J. (2015). Smoking-Related Renal Histologic Injury in IgA Nephropathy
Patients. Yonsei medical journal, 57(1), 209-16. Doi: 10.3349/ymj.2016.57.1.209
Csongradi, E., Juncos, L. A., Drummond, H. A, Vera, T. and Stec, D. E. (2012). Role of
carbon monoxide in kidney function: Is a little carbon monoxide good for the kidney?
The Curr. Pharm. Biotechnology, Vol. 13, No. 6, pp. 819-826.
Couser, W. G. and Johnson, R. J. (2014). The Etiology of Glomerulonephritis: Roles of
Infection and Autoimmunity. The International Society of Nephrology, Vol. 86, pp.
905-914. Doi: 10.1038/ki.2014.49
Farkner, B. and Kushner, H. (2008). Treatment With Metoprolol Succinate, a Selective Beta
Adrenergic Blocker, Lowers Blood Pressure Without Altering Insulin Sensitivity in
Diabetic Patients. Journal of Clinical Hypertension, 10(1):51-7. Doi: 10.1111/j.1524-
6175.2007.07458.x

HEALTH
Floege, J. and Amann, K. (2016). Acute Glomerulonephritis. The Lancet, Vol. 387, No.
10032, pp. 2036-2048. DOI: https://doi.org/10.1016/S0140-6736(16)00272-5
Friederich-Persson, M., Thörn, E., Hansell, P., Nangaku, M., Levin, M., & Palm, F. (2013).
Kidney hypoxia, attributable to increased oxygen consumption, induces nephropathy
independently of hyperglycemia and oxidative stress. Hypertension (Dallas, Tex. :
1979), 62(5), 914-9.
Irastorza, G. R., Espinosa, G., Frutos, M., Alonso, J. J., Praga, M., Parrales, L., Rivera, F.,
Marhuenda, A. R. Segarra, A. and Quereda, C. (2012). Diagnosis and treatment of
lupus nephritis. Consensus document from the systemic auto-immune disease group
(GEAS) of the Spanish Society of Internal Medicine (SEMI) and the Spanish Society
of Nephrology (S.E.N.). The Nefrologia, Vol. 32, No. 1, pp. 1-35. DOI:
10.3265/Nefrologia.pre2011.Dec.11298
Jeloka, T. K. (2012). Pathophysiology of Acute Interstitial Nephritis. The Elsevier, Vol. 1,
No. 1, pp. 27-28. Doi: https://doi.org/10.1016/S2211-9477(11)70007-3
Kovesdy, C. P. (2012). Metabolic acidosis and kidney disease: Does bicarbonate therapy
slow the progression of CKD? The Nephrol Dial Transplant, Vol. 2012, No. 27, pp.
3056-3062. Doi: 10.1093/ndt/gfs291
Mayo Clinic. (2018). Glomerulonephritis. Retrieved from:
https://www.mayoclinic.org/diseases-conditions/glomerulonephritis/diagnosis-
treatment/drc-20355710. accessed on 12/3/2019
Mok, C. C. (2012). Understanding lupus nephritis: diagnosis, management, and treatment
options. International journal of women's health, 4, 213-22.

HEALTH
McInerny, T. K., Adam, H. M., Campbell, D. E., DeWitt, T. G., Foy, J. M. and Kamat, D.
(2017). American Academy of Pediatrics Textbook of Pediatric Care. American
Academy of Pediatrics. Retrieved from:
https://pediatriccare.solutions.aap.org/book.aspx?bookid=1626. Accessed on:
12/3/2019
Naughton, C. (2008). Drug induced nephrotoxicity. American Family Physician, Vol. 78, No.
6, pp. 743-750.
Niaudet, P. (2018). Overview of the pathogenesis and causes of glomerulonephritis in
Children. Retrieved from: https://www.uptodate.com/contents/overview-of-the-
pathogenesis-and-causes-of-glomerulonephritis-in-children. Accessed on: 2/3/2019
Praga, M and Appel G. B. (2018). Clinical manifestations and diagnosis of acute interstitial
nephritis. Retrieved from: https://www.uptodate.com/contents/clinical-manifestations-
and-diagnosis-of-acute-interstitial-nephritis#H9. Accessed on 12/3/2019
Parikh, S. V., & Rovin, B. H. (2016). Current and Emerging Therapies for Lupus Nephritis.
Journal of the American Society of Nephrology: JASN, 27(10), 2929-2939. Doi:
10.1681/ASN.2016040415
Russo, G. E., Musto, T. G., Testorio, M., Molfino, A., Martinez, a., Nunzi, A, De Bon, V.,
Grynyshyv, D., D’Angelo, A., Innico, G. and Lai, S. (2014). Glomerulonephritis,
Pathogenetic Mechanisms and Therapeutic Options: An Overview. Journal of
Nwphrology & Therapeutics, ISSN: 2161-0959.
Stephens, C. (2018). Acute Nephritis. Retrieved from:
https://www.healthline.com/health/acute-nephritic-syndrome. Accessed on: 12/3/2019

HEALTH
Sandys, V., Moloney, B., Lane, L., Qazi, J., Doyle, B., Barry, M., Leavey, S. and Conlon, P.
(2018). Granulomatous interstitial nephritis secondary to adalimumab therapy,
Clinical Kidney Journal, Vol. 11, No. 2, pp. 219–221. Doi:
https://doi.org/10.1093/ckj/sfx104
Tojo, A. and Kinugasa, S. (2012). Mechanism of glomerular albumin filtration and tubular
reabsorption. The International Journal of Nephrology, Vol. 2012, Article ID 481520,
pp. 9. Doi: http://dx.doi.org/10.1155/2012/481520
Voss, B., Kurdi, A., Skopec, A., Saleh, J., El-Othmani, M. M., Lane, J. M., Mihalko, W. M.,
Saleh, K. J. (2015). Renal and Gastrointestinal Considerations in Joint Replacement
Surgery. Journal of nature and science, 1(2), e46.