How would a pneumococcal infection lead to glomerulonephritis? How can glomerulonephritis result in nephrosis?
An infection by streptococcus bacteria activates the body’s immune response towards the antigen (Rodriguez-Iturbe et al., 2016). This results in the formation of immune complexes against the antigen. The immune complex in blood circulation are deposited in the kidney glomeruli, triggering inflammation and changes in the structural architecture. Deposition of immune complexes alters the glomeruli basement membrane’s cells. This will result in increased permeability of the kidney and larger solvents such as protein will be filtered (Rodriguez-Iturbe et al., 2016).
Use JH’s laboratory values to determine if he is still experiencing nephrosis or if his condition is progressing to renal failure.
The lab results analysis: PaCO2, HCO3-, Hct 30%, Na+ 130 mEq/L, K+ 5.4 mEq/L, BUN 58 mg.dl, creatinine 3.9 mg/dl, albumin 2.0 g/dl and few traces of protein in urine indicate that the patient is progressing towards renal failure.
What additional physical or laboratory findings would be helpful in determining JH’s degree of renal impairment?
The lab findings: BUN 58 mg/dl and creatinine 3.9 mg/dl are deranged. Decreased urine output will result in fluid overload thus the patient will present with edema. Low HCO3- causes metabolic acidosis and thus result in hyperventilation with respiratory compensation (Glassock et al., 2015). The patient will present with lethargy because of low hematocrit. Serum calcium, urinalysis test are other important laboratory findings that would be of significance.
How will JH’s therapy change if his condition has progressed from nephrosis to uremia?
Nephrosis results in excessive loss of proteins and thus the patient is advised to increase the protein diet (Narang, 2015). Close monitoring of fluid intake is required. When uremia sets in, the patient will be required to reduce the protein diet. There is also a need to take precautionary measures when administering fluid to avoid volume overload as the urine output has been compromised. Sodium salt intake is also restricted to avoid fluid retention in the extravascular spaces which may worsen the symptoms (Glassock et al., 2015).
References
Glassock, R. J., Alvarado, A., Prosek, J., Hebert, C., Parikh, S., Satoskar, A., ... & Hebert, L. A. (2015). Staphylococcus-related glomerulonephritis and poststreptococcal glomerulonephritis: why defining “post” is important in understanding and treating infection-related glomerulonephritis. American Journal of Kidney Diseases, 65(6), 826- 832.
Narang, S. (2015). Acute post streptococcal glomerulonephritis. International Journal of Medical Science Research and Practice, 2(1), 56.
Rodríguez-Iturbe, B., Vaziri, N. D., Herrera-Acosta, J., & Johnson, R. J. (2016). Oxidative stress, renal infiltration of immune cells, and salt-sensitive hypertension: all for one and one for all. American Journal of Physiology-Renal Physiology, 286(4), F606-F616.