Abstract: The invention features methods for treating or reducing the likelihood of developing a renal disease by administering to a subject in need thereof an agent that decreases expression of a pathogenic APOL1. The agents of the method target various signaling pathways and decrease the level of the pathogenic APOL1 polypeptide.

Abstract: Methods are disclosed herein for detecting a genetic predisposition to focal segmental glomerulosclerosis (FSGS) or hypertensive end-stage kidney disease (ESKD) or both in a human subject. The methods include detecting the presence of at least one single nucleotide polymorphism (SNP) in an APOL1 gene, such as the C-terminal exon of an APOL1 gene. In a further embodiment, methods are disclosed for detecting resistance of a subject to a disease associated with Trypanosoma infection. The methods include detecting the presence of at least one single nucleotide polymorphism (SNP) in an APOL1 gene, such as the C-terminal exon of an APOL1 gene. Also disclosed are methods for treating a subject infected with T brucei (such as T. brucei brucei, T b. rhodesiense, or T b. gambiense). The methods include administering a therapeutically effective amount of an APOL1 protein including a S342G substitution, an I384M substitution, and/or a deletion of N388 and Y389 to the subject.

Abstract: The invention features methods for treating or reducing the likelihood of developing a renal disease by administering to a subject in need thereof an agent that decreases expression of a pathogenic APOL1. The agents of the method target various signaling pathways and decrease the level of the pathogenic APOL1 polypeptide.

Abstract: The invention features methods for treating or reducing the likelihood of developing a renal disease by administering to a subject in need thereof an agent that decreases expression of a pathogenic APOL1. The agents of the method target various signaling pathways and decrease the level of the pathogenic APOL1 polypeptide.

Abstract: Methods are disclosed herein for detecting a genetic predisposition to focal segmental glomerulosclerosis (FSGS) or hypertensive end-stage kidney disease (ESKD) or both in a human subject. The methods include detecting the presence of at least one single nucleotide polymorphism (SNP) in an APOL1 gene, such as the C-terminal exon of an APOL1 gene. In a further embodiment, methods are disclosed for detecting resistance of a subject to a disease associated with Trypanosoma infection. The methods include detecting the presence of at least one single nucleotide polymorphism (SNP) in an APOL1 gene, such as the C-terminal exon of an APOL1 gene. Also disclosed are methods for treating a subject infected with T. brucei (such as T. brucei brucei, T. b. rhodesiense, or T. b. gambiense). The methods include administering a therapeutically effective amount of an APOL1 protein including a S342G substitution, an I384M substitution, and/or a deletion of N388 and Y389 to the subject.

Abstract: Methods are disclosed herein for detecting a genetic predisposition to focal segmental glomerulosclerosis (FSGS) or hypertensive end-stage kidney disease (ESKD) or both in a human subject, e.g., by detecting the presence of at least one single nucleotide polymorphism (SNP) in an APOL1 gene, such as the C-terminal exon of an APOL1 gene. In a further embodiment, methods are disclosed for detecting resistance of a subject to a disease associated with Trypanosoma infection, e.g., by detecting at least one single nucleotide polymorphism (SNP) in an APOL1 gene, such as the C-terminal exon of an APOL1 gene. Also disclosed are methods for treating a subject infected with T. brucei. The methods include administering a therapeutically effective amount of an APOL1 protein including a S342G substitution, an I384M substitution, and/or a deletion of N388 and Y389 to the subject.

Abstract: The invention features methods for treating or reducing the likelihood of developing a renal disease by administering to a subject in need thereof an agent that decreases expression of a pathogenic APOL1. The agents of the method target various signaling pathways and decrease the level of the pathogenic APOL1 polypeptide.

Abstract: Compositions and methods are disclosed herein for treating or reducing the symptoms of a renal disease, such as focal segmental glomerulosclerosis (FSGS), hypertensive end-stage kidney disease (ESKD), and HIV-associated nephropathy (a distinct form of FSGS, also termed collapsing glomerulopathy). The compositions include the common variant of APOL1 and fragments thereof, as well as antibodies and fragments thereof that bind and neutralize pathogenic APOL1, nucleic acid molecules that encode the common variant of APOL1 and fragments thereof, and other compounds that bind and neutralize pathogenic APOL1. The methods of the invention include administering one or more of the compositions of the invention to a subject having or at risk of developing renal disease.

Abstract: Methods are disclosed herein for detecting a genetic predisposition to focal segmental glomerulosclerosis (FSGS) or hypertensive end-stage kidney disease (ESKD) or both in a human subject, e.g., by detecting the presence of at least one single nucleotide polymorphism (SNP) in an APOL1 gene, such as the C-terminal exon of an APOL1 gene. In a further embodiment, methods are disclosed for detecting resistance of a subject to a disease associated with Trypanosoma infection, e.g., by detecting at least one single nucleotide polymorphism (SNP) in an APOL1 gene, such as the C-terminal exon of an APOL1 gene. Also disclosed are methods for treating a subject infected with T. brucei. The methods include administering a therapeutically effective amount of an APOL1 protein including a S342G substitution, an I384M substitution, and/or a deletion of N388 and Y389 to the subject.

Abstract: Compositions and methods are disclosed herein for treating or reducing the symptoms of a renal disease, such as focal segmental glomerulosclerosis (FSGS), hypertensive end-stage kidney disease (ESKD), and HIV-associated nephropathy (a distinct form of FSGS, also termed collapsing glomerulopathy). The compositions include the common variant of APOL1 and fragments thereof, as well as antibodies and fragments thereof that bind and neutralize pathogenic APOL1, nucleic acid molecules that encode the common variant of APOL1 and fragments thereof, and other compounds that bind and neutralize pathogenic APOL1. The methods of the invention include administering one or more of the compositions of the invention to a subject having or at risk of developing renal disease.

Abstract: Compositions and methods are disclosed herein for treating or reducing the symptoms of a renal disease, such as focal segmental glomerulosclerosis (FSGS), hypertensive end-stage kidney disease (ESKD), and HIV-associated nephropathy (a distinct form of FSGS, also termed collapsing glomerulopathy). The compositions include the common variant of APOL1 and fragments thereof, as well as antibodies and fragments thereof that bind and neutralize pathogenic APOL1, nucleic acid molecules that encode the common variant of APOL1 and fragments thereof, and other compounds that bind and neutralize pathogenic APOL1. The methods of the invention include administering one or more of the compositions of the invention to a subject having or at risk of developing renal disease.